dissertation topics rheumatoid arthritis

Rheumatoid Arthritis: Pathogenesis and Target-Treatments

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Literature review of rheumatoid arthritis in India

Affiliations.

• 1 Indraprastha Apollo Hospital, New Delhi, India.
• 2 Sri Deepti Rheumatology Centre, Hyderabad, India.
• 3 Evidera, Meta Research, Lexington, MA, USA.
• 4 Pfizer Inc., Mumbai, India.
• 5 Pfizer Inc., New York, NY, USA.
• PMID: 26171649
• DOI: 10.1111/1756-185X.12621

Aim: Rheumatoid arthritis (RA) can lead to severe disability. This literature review assessed the descriptive epidemiology, comorbidities and extra-articular manifestations, functioning abilities and quality of life, and treatment patterns of RA patients in India.

Method: A literature review of all observational studies published from 1985 to 2012 was conducted using MEDLINE and Embase. Quantitative and qualitative findings were summarized.

Results: Twenty-eight studies were identified for data extraction. Seven described the descriptive epidemiology of RA, 14 described comorbidities and extra-articular manifestations, nine described the functioning abilities and quality of life among patients, and 10 provided information on treatments.

Conclusion: This review is confined to studies with small sample sizes, cross-sectional designs, and/or clinical settings that may not be representative of the entire Indian population. There is a need for more robust studies, as conclusions for the entire Indian RA population cannot be drawn from only the current observational studies.

Keywords: India; literature review; rheumatoid arthritis.

© 2015 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd.

Publication types

• Antirheumatic Agents / adverse effects
• Antirheumatic Agents / therapeutic use*
• Arthritis, Rheumatoid / diagnosis
• Arthritis, Rheumatoid / drug therapy*
• Arthritis, Rheumatoid / epidemiology
• Comorbidity
• Disability Evaluation
• India / epidemiology
• Observational Studies as Topic
• Risk Factors
• Severity of Illness Index
• Treatment Outcome
• Antirheumatic Agents

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Home > STUDENTWORK > HONORS-THESIS > 81

Honors Thesis

Rheumatoid Arthritis: A Literature Review and Comprehensive Treatment Analysis

Charlton Mechling , University of South Dakota Follow

Date of Award

Spring 4-24-2020

Document Type

Department/major.

Health Science

First Advisor

Jonelle Hook

Second Advisor

Jamie Turgeon-Drake

Third Advisor

Rheumatoid Arthritis, Autoimmune, Treatment, Survey

Subject Categories

Diseases | Medicine and Health Sciences

Rheumatoid arthritis (RA) is a systemic and debilitating autoimmune disease. The varying levels of severity of rheumatoid arthritis make it notably unique. Rheumatoid arthritis is not strictly an inflammatory disease of the joints; it is an extensive disease with many extra-articular manifestations that complicate its treatment and management. In addition to being a disease that is internally driven by the body’s immune system, current research reveals the pervasive influence of environmental factors on the disease’s severity and activity. This literature review examines the pathophysiology of RA, its implications on the body, and current treatment options to ameliorate some of its symptoms and complications. A particular focus on the efficacy and potential value of diet, psychosocial interventions, physical activity, and therapeutic modalities is central to the current work. Evidence using a literature review of peer-reviewed articles discussing RA and its many facets is utilized. A survey of patients with RA reveals patient attitudes and discretions towards their arduous personal experiences with rheumatoid arthritis. Overall, the findings indicate that having a well-versed interprofessional team of physicians and health professionals supporting patients with rheumatoid arthritis using an integrated model of care, is critical to improved overall well-being and disease outcomes.

Recommended Citation

Mechling, Charlton, "Rheumatoid Arthritis: A Literature Review and Comprehensive Treatment Analysis" (2020). Honors Thesis . 81. https://red.library.usd.edu/honors-thesis/81

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Extra-articular Manifestations in Rheumatoid Arthritis

Manole cojocaru.

a "Titu Maiorescu" University, Faculty of Medicine, Discipline of Physiology, Center for Rheumatic Diseases, Bucharest, Romania

Inimioara Mihaela Cojocaru

b "Carol Davila" University of Medicine and Pharmacy, Department of Neurology, Colentina Clinical Hospital, Bucharest, Romania

Isabela Silosi

c University of Medicine and Pharmacy, Faculty of Medicine, Discipline of Immunology, Craiova, Romania

Camelia Doina Vrabie

d "Carol Davila" University of Medicine and Pharmacy, Clinical Hospital of Emergency "Sfantul Ioan", "Victor Babes" National Institute for Pathology and Biomedical Sciences, Bucharest, Romania

R Tanasescu

Rheumatoid arthritis (RA) is a systemic autoimmune disease whose main characteristic is persistent joint inflammation that results in joint damage and loss of function.

Although RA is more common in females, extra-articular manifestations of the disease are more common in males. The extra-articular manifestations of RA can occur at any age after onset. It is characterised by destructive polyarthritis and extra-articular organ involvement, including the skin, eye, heart, lung, renal, nervous and gastrointestinal systems. The frequence of extra-articular manifestations in RA differs from one country to another. Extra-articular organ involvement in RA is more frequently seen in patients with severe, active disease and is associated with increased mortality. Incidence and frequence figures for extra-articular RA vary according to study design. Extra-articular involvement is more likely in those who have RF and/or are HLA-DR4 positive. Occasionally, there are also systemic manifestations such as vasculitis, visceral nodules, Sjögren's syndrome, or pulmonary fibrosis present. Nodules are the most common extra-articular feature, and are present in up to 30%; many of the other classic features occur in 1% or less in normal clinic settings. Sjögren's syndrome, anaemia of chronic disease and pulmonary manifestations are relatively common – in 6-10%, are frequently present in early disease and are all related to worse outcomes measures of rheumatoid disease in particular functional impairment and mortality. The occurrence of these systemic manifestations is a major predictor of mortality in patients with RA.

This paper focuses on extra-articular manifestations, defined as diseases and symptoms not directly related to the locomotor system.

R Rheumatoid arthritis (RA) is the most common inflammatory joint disease, affecting 1-2% of the population world­wide, with women affected two to three times more commonly than men ( 1 ). Rheumatoid arthritis is a systemic inflammatory disease that can involve other tissues and organs as well as synovial joints. Rheumatoid arthritis is an inflammation of synovial tissue with symmetric involvement of peripheral joints, hand, feet, and wrists being most commonly affected. Rheumatoid arthritis can also affect non-articular muscular structures such as tendons, ligaments, and fascia ( 2 ).

Rheumatoid arthritis is associated with a high risk for morbidity and premature death secondary to the earlier development of cardiovascular, lung diseases and malignancy ( 3 ). Recent epidemiologic studies of extra-articular RA manifestations have emphasized their major role as predictors of premature mortality in patients with RA ( 4 ). Extra-articular manifestations are all the conditions and symptoms which are not directly related to the locomotor system ( 2 , 4 , 5 ).

Extra-articular RA is a serious condition, and rheumatoid arthritis patients with extra-articular manifestations should be aggressively treated and monitored ( 6 ). Extra-articular manifestations of RA occur in about 40% of patients, either in the beginning or during the course of their disease ( 7 ). There is no agreed classification for these manifestations and, because criteria and definitions vary so much, this paper includes not only the classic extra-articular features, but also the non-articular complications of RA, for example normochronic normocytic anaemia and chronic leg ulcers, and the important disease-associated comorbidities, including non-Hodgkin's lymphoma, ischaemic heart disease and osteoporosis ( 8 ). Systemic features in RA are frequent, mostly related to vasculitis, and often a reflection of longstanding inflammation. Most organs can be involved ( 9 , 10 ). These manifestations occur as frequent in men as in women, and may appear at any age. Many of these manifestations are related to the more active and severe RA, so early and more aggressive RA drug therapies are being employed and, although evidence from randomised studies is not available, this approach would seem appropriate in view of the adverse effect of extra-articular manifestations on RA outcomes ( 3 , 4 , 11 , 12 ).

Patients with RA, who have high titers of rheumatoid factor (ie, autoantibodies to the Fc component of immunoglobulin G are most likely to have extra-articular manifestations of their disease, including rheumatoid nodules, rheumatoid vasculitis, and pleuropulmonary, neurologic, digestive, cardiovascular, cutaneous, hematologic, and ocular complications ( 13 - 15 ). Rheumatoid arthritis is one of the most prevalent connective tissue diseases and can be complicated by vasculitis with systemic manifestations ( 16 , 17 ). The prevalence of extraarticular manifestations of RA has declined in recent years, with the timing and pattern of the decline indicating that disease-modifying RA treatments may be changing the natural history of the disease ( 18 - 20 ).

Advances in the understanding of the pathogenesis of RA and development of new, more specific drugs may be of particular benefit to patients with extra-articular disease ( 21 , 22 ). Trends for specific extra-articular manifestations varied, showing liner declines in fibromyalgia syndrome, increases in RA lung disease (possible reflecting increased diagnostic sensitivity), and significant breakpoint declines in carditis and pooled serious extra-articular manifestations. Early recognition and treatment are important to decrease mortality ( 23 , 24 ).

This paper will briefly review extra-articular manifestations of RA with an emphasis on recent clinical research. ❑

SKIN MANIFESTATIONS

Rheumatoid nodules are the most frequent skin manifestations (20%) in RA. They occur mainly in rheumatoid factor positive RA patients and in early RA give risk to severe extra-articular manifestations. Histologically focal central fibrinoid necrosis with surrounding fibroblasts is observed: it is believed to occur as a result of small vessel vasculitis. Other manifestations of rheumatoid small vessel vasculitis affecting the skin are splinter haemorrhages, periungual infarcts, leg ulcers, digital gangrene and sharply demarcated painful ulcerations. They appear mostly at the lower extremities or where skin is exposed to pressure.

Skin manifestations are frequently associated with episcleritis, pleural and pericardial effusions. Early lesions show fibrinoid necrosis of the vessel wall, with an inflammatory cell infiltrate. Later on, artery wall fibrosis with occlusion can appear. Subcutaneous nodules commonly occur on extensor surfaces subject to extenal pressure, for example, the upper forearm and elbow. Occasionally, they arise within the lungs or heart. Nodules are rare in seronegative RA ( 1 - 4 , 25 - 27 ). Pyoderma gangrenosum is a rare disease characterized by chronic, recurrent ulceration of non-infective origin and usually associated with rheumatoid arthritis. Pyoderma gangrenosum is a circumscribed necrotizing vasculitis of unknown etiology. Lesions associated with arthritis are often ulcerative. Although these lesions typically affect the lower limbs, they can also affect the entire body ( 28 , 29 ). ❑

OCULAR MANIFESTATIONS

The most frequent is keratoconjunctivitis sicca, which affects at least 10% of patients. It is frequently observed together with xerostomia in a secondary Sjögren's syndrome ( 3 ). Episcleritis, inflammation of the layer superficial to the sclera, occurs in less than 1% of patients with RA and is generally a self-limiting condition. Scleritis is a more aggressive process, characterized by an intensely painful inflammation of the sclera itself. Peripheral ulcerative keratitis develops as an extension of scleral inflammation with involvement of the peripheral cornea and can lead to corneal melt ( 1 , 2 , 4 , 30 , 31 ). ❑

ORAL MANIFESTATIONS

Oral dryness and salivary gland swelling can also be found in patients with RA. These patients can also develop secondary Sjögren's syndrome ( 3 ). ❑

GASTROINTESTINAL SYSTEM

Gastrointestinal complications in RA are mostly iatrogenic and caused by medications. Primary involvement of the gastrointestinal tract, caused by mesenteric vasculitis leading to intestinal infarction, is very rare ( 3 ). This condition causes acute abdominal pain, and can lead to intestinal bleeding and perforation. There is no direct relation with arthritis activity, but as with other vasculitis, it is mostly observed in RA patients with high rheumatoid factor and subcutaneous nodules. Prognosis is poor and outcome frequently fatal ( 1 , 2 , 4 ). ❑

PULMONARY MANIFESTATIONS

Pulmonary involvement in RA is frequent although not always clinically recognized. Pleural disease is common but usually asymptomatic; autopsy studies reported pleural involvement in 50% of cases, with only 10% clinically detected ( 5 , 32 - 35 ). Pleural effusions are usually exudates with mixed cell counts and high protein concentration. Multinucleated giant cells are highly specific but seen in fewer than 50% of the cases ( 6 , 36 - 38 ). The disease is frequently associated with exsudative pericarditis, and with interstitial lung disease. Parenchimal pulmonary nodules generally are asymptomatic and found in RF-positive patients with nodules elsewhere ( 7 , 8 , 39 ). They can cavitate and cause pleural effusions. Pathological examination of the nodules reveals a central necrotic zone surrounded by a cellular area of proliferating fibroblasts ( 40 ). As with classical subcutaneous nodules, the underlying process appears to be a vasculitis. Interstitial lung disease is associated with RA; however, the prevalence and natural history are undefined. Diffuse interstitial pulmonary fibrosis in RA tends to occur more often in RF-positive male patients with longstanding nodular disease ( 9 , 10 , 41 - 43 ). ❑

CARDIAC DISEASE

Rheumatoid arthritis patients are also more prone to heart conditions like the thickening of the artery walls (atherosclerosis) and heart attacks ( 44 ). Extra-articular manifestations of RA and the presence of traditional cardiovascular risk factors were also found. The risk for myocardial infarction in female RA patients is twice that of women without RA, and in long-standing disease of at least 10 years, the risk is 3 times higher. Pericaditis is the most common cardiac manifestation in RA ( 45 - 48 ). Although symptomatic pericarditis is relatively uncommon, autopsy studies revealed evidence of pericardial inflammation in 50% of the patients. It usually occurs in RF-positive patients with nodules and analysis of pericardial fluid reveals changes similar to those found in rheumatoid pleural effusions ( 49 ). Myocarditis (with presence of rheumatoid nodules) has been observed in autopsy studies, and myocardial fibrosis can lead to conduction abnormalities. Congestive heart failure may be more frequent than is clinically evident in RA ( 50 ). Endocarditis with formation of rheumatoid nodules in the aortic or mitral valves can lead to valvular dysfunction. Arterial stiffness is an important factor in cardiovascular comorbidity in patients with RA. Rheumatoid arthritis is associated with decreased distensibility of the abdominal aorta in females, and such changes seem to correlate with disease severity ( 1 - 4 , 51 - 53 ). ❑

RENAL DISEASE

Renal involvement in RA is rare, mesangial glomerulonephritis was the most common histopathological finding, whereas amyloidosis was the most common finding among patients with nephritic syndrome. Glomerulonephritis and interstitial renal disease are uncommon in the absence of vasculitis ( 3 ). Renal abnormalities are frequently iatrogenic ( 1 , 2 , 4 ). ❑

NEUROLOGICAL MANIFESTATIONS

Peripheral neuropathy, presenting as diffuse sensorimotor neuropathy or mononeuritis multiplex, occurs in a small subset of patients with RA. The underlying mechanism is small vessel vasculitis of the vasa vasorum of the nerves with ischemic neuropathy and demyelinisation. These manifestations are part of the rheumatoid vasculitis syndrome. Cervical myelopathy, caused by atlantoaxial subluxation or pannus formation, occurs frequently in RA patients with severe and longstanding disease ( 7 , 54 , 55 ). ❑

HAEMATOLOGIC MANIFESTATIONS

Patients with RA may present with haematological abnormalities either at the time of diagnosis, or during the course of their illness. Haematological manifestations in RA can be broadly categorized into areas of anaemia, neutropenia, thrombocytopenia, thrombocytosis, eosinophilia, and haematological malignancies ( 56 ). Anaemia is, by far, one of the most common extra-articular symptoms of RA. The cause of anaemia in RA is multifactorial-disease activity, drug-induced, nutritional, gastrointestinal bleed, bone marrow suppression, and ineffective erythopoesis ( 57 ). Anaemia of chronic disease is observed in RA, where it usually correlates with the disease activity, particular the degree of articular inflammation. It is normochromic and normocytic. Eosinophilia in RA reflects active disease or hypersensitivity to drugs ( 58 ). Thrombocytosis is a frequent finding in active RA and is correlated with the number of active inflamed joints ( 59 ). Lymphadenopathy is sometimes observed in active RA, usually presenting on biopsy as benign follicular hyperplasia ( 12 - 14 , 60 ). ❑

CONCLUSIONS

Rheumatoid arthritis is a chronic systemic disease of unknown etiology characterized by articular involvement, extra-articular involvement, and the presence of serum rheumatoid factor. In RA, there is a symmetric and persistent inflammation of the synovial tissue, usually involving the peripheral joints. Although considered a "joint disease" rheumatoid arthritis is associated with involvement of extra-articular manifestations. Prevalence of these manifestations is about 40% of patients at any time during the course of the disease; almost all manifestations are a consequence of longstanding active disease (vasculitis). Extra-articular RA is a serious condition, and RA patients with extra-articular manifestations should be aggressively treated and monitored. Currently, there are no reliable predictors for these features in early RA, although they are associated with men, smokers, more severe joint disease, and worse function. The longer the duration of the disease will be, the larger the number of extra-articular manifestations. Extra-articular manifestations in RA were present in a substantial proportion of patients, which lead to a worse disease outcome. Anaemia, thrombocytosis and respiratory system involvement were the commonest. They need to be recognised early and managed promptly. ❑

Rheumatoid Arthritis: A Psychological Intervention

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A psychological intervention involving relaxation training and biofeedback training for the control of peripheral skin temperature was investigated in this study with 27 female rheumatoid arthritics as participants. Based on analysis of the temperature data, it was concluded that the biofeedback response was not learned. From electromyographic data, it was concluded that participants did learn to relax. The hypothesis that the two treatment components would have beneficial effects on the physical, functional, and psychological aspects of rheumatoid arthritis was answered partially. No differential effects as a function of biofeedback training were found as the data for the temperature increase and … continued below

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McGraw, Phillip C., 1950- May 1979.

This dissertation is part of the collection entitled: UNT Theses and Dissertations and was provided by the UNT Libraries to the UNT Digital Library , a digital repository hosted by the UNT Libraries . It has been viewed 18809 times, with 232 in the last month. More information about this dissertation can be viewed below.

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• McGraw, Phillip C., 1950-
• Lawlis, G. Frank Major Professor

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• Haynes, Jack Read
• Stricklin, Annie B.
• Butler, Joel R.
• Critelli, Joseph W.
• Achterberg, Gloria Jeanne
• North Texas State University Place of Publication: Denton, Texas

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• Department: Department of Psychology
• Discipline: Clinical Psychology
• Level: Doctoral
• Name: Doctor of Philosophy
• PublicationType: Doctoral Dissertation
• Grantor: North Texas State University

A psychological intervention involving relaxation training and biofeedback training for the control of peripheral skin temperature was investigated in this study with 27 female rheumatoid arthritics as participants. Based on analysis of the temperature data, it was concluded that the biofeedback response was not learned. From electromyographic data, it was concluded that participants did learn to relax. The hypothesis that the two treatment components would have beneficial effects on the physical, functional, and psychological aspects of rheumatoid arthritis was answered partially. No differential effects as a function of biofeedback training were found as the data for the temperature increase and temperature decrease groups were statistically combined in multiple analyses of variance for repeated measures. Although no differential effects were obtained, numerous positive changes were found. Correlated with the relaxation training were decreases in reported subjective units of discomfort, percentage of time hurting, percentage of body hurting, and general severity of pain. Improved sleep patterns were reported as was increased performance of activities of daily living. Reductions were also found in psychological tension, and in the amount of time mood was influenced by the disease. Shifts were not found in imagery, locus of control, and other psychological dimensions. Constitutional improvements were also absent.

• biofeedback training
• chronic pain
• relaxation training
• rheumatoid arthritis

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RSC Medicinal Chemistry

A new class of 7-deazaguanine agents targeting autoimmune diseases: dramatic reduction of synovial fibroblast il-6 production from human rheumatoid arthritis patients and improved performance against murine experimental autoimmune encephalomyelitis †.

* Corresponding authors

a School of Chemistry, Trinity College, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Dublin, Ireland E-mail: [email protected] , [email protected]

b School of Biochemistry & Immunology, Trinity College, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Dublin, Ireland E-mail: [email protected]

c School of Medicine, Trinity College, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Dublin, Ireland

A simple in vitro assay involving the measurement of IL-6 production in human synovial fibroblasts from rheumatoid arthritis patients has been utilised to select candidates from a targeted library of queuine tRNA ribosyltransferase (QTRT) substrates for subsequent in vivo screening in murine experimental autoimmune encephalomyelitis (EAE – a model of multiple sclerosis). The in vitro activity assay discriminated between poor and excellent 7-deazaguanine QTRT substrates and allowed the identification of several structures which subsequently outperformed the previous lead in EAE. Two molecules were of significant promise: one rigidified analogue of the lead, and another considerably simpler structure incorporating an oxime motif which differs structurally from the lead to a considerable extent. These studies provide data from human cells for the first time and have expanded both the chemical space and current understanding of the structure–activity relationship underpinning the remarkable potential of 7-deazguanines in a Multiple Sclerosis disease model.

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A new class of 7-deazaguanine agents targeting autoimmune diseases: dramatic reduction of synovial fibroblast IL-6 production from human rheumatoid arthritis patients and improved performance against murine experimental autoimmune encephalomyelitis

M. Cotter, S. M. Quinn, U. Fearon, S. Ansboro, T. Rakovic, J. M. Southern, V. P. Kelly and S. J. Connon, RSC Med. Chem. , 2024, Advance Article , DOI: 10.1039/D4MD00028E

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Billing and Coding: MolDX: Molecular Biomarker Testing to Guide Targeted Therapy Selection in Rheumatoid Arthritis

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• Rheumatoid Arthritis

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Page Help for Article - Billing and Coding: MolDX: Molecular Biomarker Testing to Guide Targeted Therapy Selection in Rheumatoid Arthritis (A59536)

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Dissertations / Theses on the topic 'Rheumatoid arthritis, T cell'

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Hildalgo, Ester. "T cells in Rheumatoid Arthritis." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1715/.

Schatz, Annika Katrin. "Homöostatische Mechanismen der CD4+ T-Zellgenese bei Rheumatoider Arthritis." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-215633.

Cornelis, Francois Baptiste. "Contributions of T-cell receptor genes to rheumatoid arthritis susceptibility." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239712.

Kamarova, Halina. "CD4+161+ T Cells in Rheumatoid Arthritis." Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490658.

Walter, Gina. "Do activated monocytes impair regulatory T cell function in rheumatoid arthritis?" Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/do-activated-monocytes-impair-regulatory-t-cell-function-in-rheumatoid-arthritis(bec96e89-858a-42a3-87cf-6167ee9d633e).html.

Barth, Jan Thomas. "Hyporesponsive synovial fluid T-cells in rheumatoid arthritis." [S.l.] : [s.n.], 2003. http://www.freidok.uni-freiburg.de/volltexte/816.

Berg, Louise. "Functional studies of T-cells in rheumatoid arthritis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4314-1/.

Lawson, Catherine Ann. "CD4+CD25high regulatory T cells in rheumatoid arthritis." Thesis, University of Leeds, 2008. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496533.

Bowman, Simon Jonathan. "Immunogenetic and T cell receptor repertoire studies in Felty's syndrome." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362715.

Pirronello, Fausto [Verfasser], and Alla [Akademischer Betreuer] Skapenko. "Altered T cell plasticity favors Th17 cells in rheumatoid arthritis / Fausto Pirronello ; Betreuer: Alla Skapenko." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1202011888/34.

Ibberson, Mark Robert. "Genomic organisation and polymorphism of the human T cell receptor variable alpha gene cluster." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321749.

Lyndon, Gavin James. "T-lymphocyte/monocyte interactions controlling cytokine release in rheumatoid arthritis." Thesis, University of Bath, 2000. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323603.

Smith, Mark Duncan. "An investigation into mycobacteria reactive T-cells in rheumatoid arthritis." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244161.

Beavis, Paul. "The phenotype and function of CD4 CD25 regulatory T cells in cytokine-activated T cell populations : relevance to rheumatoid arthritis." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521124.

Brzezinski, Jennifer Lynn. "THE ROLE OF T CELL RECEPTOR Vβ GENE POLYMORPHISMS IN SUSCEPTIBILITY TO JUVENILE RHEUMATOID ARTHRITIS." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin997381866.

Langley, Russell Stuart. "Molecular characterisation of NK cells and T lymphocytes in rheumatoid arthritis." Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421066.

Lopes, Ana Paula Pinheiro. "Expression of CXCR3 in different T cells subsets in rheumatoid arthritis." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15471.

Kobayashi, Shio. "A Distinct Human CD4+ T cell Subset That Secretes CXCL13 in Rheumatoid Synovium." Kyoto University, 2016. http://hdl.handle.net/2433/215216.

Robey, Ian Forrest. "Binding and functional properties of natural anti-T cell receptor antibodies in patients with rheumatoid arthritis." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/289736.

Smith, Nicola Marianne Godwin. "Characterisation of T cell surface phenotype and effector function in a surrogate model of rheumatoid arthritis." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/4391.

Nadkarni, Suchita. "Regulatory T cells in rheumatoid arthritis : clinical relevance and mechanisms in disease." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1446129/.

Andersson, Ida E. "Modified Glycopeptides Targeting Rheumatoid Arthritis : Exploring molecular interactions in class II MHC/glycopeptide/T-cell receptor complexes." Doctoral thesis, Umeå universitet, Kemiska institutionen, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42082.

Mori, Masato. "Cell-contact dependent activation of CD4+ T cells by adhesion molecules on synovial fibroblasts." Kyoto University, 2017. http://hdl.handle.net/2433/218010.

Cribbs, Adam. "The phenotype and function of CD²⁵⁺CD¹²⁷⁻ regulatory T cells in rheumatoid arthritis." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18039.

Cao, Duojia. "CD25+CD4+ regulatory T cells in rheumatic disease /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-178-4/.

Gibson, Kathryn. "The pathogenic potential of endogenous-self reactive CD4 T cells in collagen-induced arthritis." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313722.

Fasth, Andreas. "CD28null T cells in rheumatoid arthritis and inflammatory myopathies : cellular characterization and clinical relevance /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-351-1/.

Nijjar, Jagtar Singh. "Macrophages and CD4 T-cells in rheumatoid arthritis and their modulation by JAK inhibitors." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/7543/.

Haupt, Sonja [Verfasser], and Alla [Akademischer Betreuer] Skapenko. "Analysis of molecular mechanisms contributing to regulatory T cell phenotype : implications for rheumatoid arthritis / Sonja Haupt. Betreuer: Alla Skapenko." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1101343931/34.

Taylor, Peter Charles. "A study of autoimmune arthritis using xenografts of human immune cells and allografts of murine immune cells into mice with severe combined immunodeficiency." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338516.

Holm, Lotta. "The MHC-glycopeptide-T cell interaction in collagen induced arthritis : a study using glycopeptides, isosteres and statistical molecular design in a mouse model for rheumatoid arthritis." Doctoral thesis, Umeå : Department of Chemistry, Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-899.

Quandt, Dagmar, and Ulf Wagner. "Peripheral CD4CD8 double positive T cells with a distinct helper Cytokine profile are increased in rheumatoid arthritis." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142667.

Yabuta, Paula Barbim Donate. "O papel dos microRNAs de células T na susceptibilidade/resistência a artrite reumatóide experimental." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-16022012-150623/.

Ito, Yoshinaga. "γδ T cells are predominant source of IL-17 in the affected joints of collagen-induced arthritis, but not in rheumatoid arthritis." Kyoto University, 2009. http://hdl.handle.net/2433/126448.

Gustafsson, Tomas. "Asymmetric Synthesis of C-Glycosylated Amino Acids : Incorporation in Collagen Glycopeptides and Evaluation in a Model for Rheumatoid Arthritis." Doctoral thesis, Umeå : Univ, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-623.

Eriksson, Catharina. "Immunological mechanisms in systemic autoimmunity : autoantibodies and chemokines in systemic lupus erythematosus and during treatment with TNF inhibitors in rheumatoid arthritis." Doctoral thesis, Umeå universitet, Klinisk immunologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42954.

Bryant, Jane. "The role of CXCR4/SDF-1 and VLA-4/VCAM-1 in migration of bystander-activated T cells : implications for rheumatoid arthritis." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7098.

Peres, Raphael Sanches. "A sinalização de TGF-β envolvida na expressão de CD39 em células T reguladoras está associada com a eficácia terapêutica do metotrexato na artrite reumatóide." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-06012017-163133/.

Schubert, David. "Arthritisinduktion durch Immunität gegen ein systemisch exprimiertes Autoantigen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2005. http://dx.doi.org/10.18452/15271.

Abdel-Nour, A. N. "Cell mediated immunity in rheumatoid arthritis." Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375007.

Pritchard, M. L. "Psychological aspects of rheumatoid arthritis." Thesis, University of Exeter, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381050.

McKee, Hayley Jane. "Aggrecan as a candidate autoantigen in rheumatoid arthritis." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323445.

Williams, Ruth J. "Is the neutrophil an inflammation signalling cell in rheumatoid arthritis?" Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337695.

Brown-Galatola, Catherine Helen. "Immunoregulation mediated by cell surface sulphydryl groups in rheumatoid arthritis." Thesis, University of Bath, 1989. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328744.

Majkowska, Iwona. "Role of DDR2 in synovial cell invasion : implications for rheumatoid arthritis." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/26900.

Rouzière, Anne-Sophie. "Modulation of the B-cell repertoire in rheumatoid arthritis by transient B-cell depletion." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973381914.

Rooke, Kelly. "Identification of chromatin modifying mechanisms in inflammatory macrophages in rheumatoid arthritis." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:e39a5b64-a72c-4bd9-ab4d-957e9b2afc53.

Wheater, Gillian G. "The effects of B cell depletion on bone turnover in rheumatoid arthritis." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3834.

Kadioglu, Aras. "Studies on mononuclear cell adhesion to mucosal endothelial cells in rheumatoid arthritis." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35389.

Baecklund, Eva. "Associations Between Rheumatoid Arthritis and Malignant Lymphomas." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5928.