An updated overview of immune complex mediated rheumatoid arthritis

Solai Sophia, Mudigere Maligaiah Ramesha

Abstract


Rheumatoid arthritis is a widely known autoimmune disorder which affects the joints and cause major disability in affected population. Even though more emphasis is given in the western world for autoimmune research, people in developing countries are also suffering significantly due to autoimmune arthritis. This review is focused on the updates in rheumatoid arthritis research and developments in therapeutic strategies. The exact cause of this disease is unknown but primary cause for inflammatory changes in the joints are considered due to cytokine network imbalance and correcting this imbalance possibly will cure the disease. Using this knowledge the newer therapeutic approaches to rheumatoid arthritis are being aimed at correcting this imbalance. Recently three most promising therapeutic products appear to be the use of monoclonal antibodies to TNF-α, soluble TNF-α receptors, and IL-1 receptor antagonist. Other therapeutic agents that could regulate the cytokine network are in various stages of laboratory and clinical evaluation. But the need to study the causative factor and prognostic marker along with other approaches is much more important to prevent clinical remission and for the complete cure of the disease. This review highlights the important recent breakthrough in the field and some suggestions for significant basic research.


Keywords


Arthritis, Autoimmune, Cytokines, Prognostic marker

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References


Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA et al. Estimates of the prevalence of arthritis and other rheumatoid conditions in the united states. part II. Arthrit Rheum. 2008;58(1):26-35.

Lundkvist J, Kastang F, Kobelt G. The burden of rheumatoid arthritis and access to treatment: health burden and costs. Eur J Health Econ. 2008;8(Suppl 2):S49-60.

Connelly LB, Woolf A, Brooks P. Cost effectiveness of interventions for musculoskeletal conditions. In: Jamison DT, Bremen JG, Measham AR, eds. Disease Control Priorities in Developing Countries. 2nd ed. New York: Oxford University Press; 2006: 963-980.

Symmons D, Turner G, Webb R, Asten P, Barrett E, Lunt M et al. The prevalence of rheumatoid arthritis in the United Kingdom: new estimates for a new century. Rheumatol (Oxford). 2002;41:793-800.

Jordan K, Clarke AM, Symmons DP, Fleming D, Porcheret M, Kadam UT et al. Measuring disease prevalence: a comparison of musculoskeletal disease using four general practice consultation databases. Br J Gen Pract. 2007;57(534):7-14.

Rodriguez LA, Tolosa LB, Ruigomez A, Johansson S, Wallander MA. Rheumatoid arthritis in UK primary care: incidence and prior morbidity. Scand J Rheumatol. 2009;38:173-7.

Choy E. Panayi G. Cytokine pathways and joint inflammation in rheumatoid arthritis. N Eng J Med. 2001;344(12):907-15.

Gonzalez A, Icen M, Kremers HM, Crowson CS, Davis JM, Therneau TM. Mortality trends in rheumatoid arthritis: the role of rheumatoid factor. J Rheumatol. 2008;35(6):1009-14.

Levy L, Fautrel B, Barnetche T, Schaeverbeke T. Incidence and risk of fatal myocardial infarction and stroke events in rheumatoid arthritis patients: a systematic review of the literature. Clin Exp Rheumatol. 2008;26:673-9.

Kaiser R. Incidence of lymphoma in patients with rheumatoid arthritis: a systematic review of the literature. Clin Lymphoma Myeloma. 2008;8:87-93.

Khurana R, Wolf R, Berney S, Caldito G, Hayat S, Berney SM. Risk of development of lung cancer is increased in patients with rheumatoid arthritis: a large case control study in US veterans. J Rheumatol. 2008;35:1704-8.

Chakravarty EF, Michaud K, Wolfe F. Skin cancer, rheumatoid arthritis, and tumor necrosis factor inhibitors. J Rheumatol. 2005;32:2130-5.

Firestein GS, Zvaifler NJ. How important are T cells in chronic rheumatoid synovitis? T cell-independent mechanisms from beginning to end. Arthrit Rheum. 2002;46:298-308.

Bombara MP, Webb DL, Conrad P, Marlor CW, Sarr T, Ranges GE et al. Cell contact between T cells and synovial fibroblasts causes induction of adhesion molecules and cytokines. J Leukoc Biol. 1993;54(5):399-406.

Dayer JM, Graham R, Russell G, Krane SM. Collagenase production by rheumatoid synovial cells: stimulation by a human lymphocyte factor. Sci. 1977;195:181-3.

Paleolog EM. Angiogenesis in rheumatoid arthritis. Arthrit Res. 2002;4(3):S81-90.

Burrage PS, Mix KS, Brinckerhoff CE. Matrix metalloproteinases: role in arthritis. Front Biosci. 2006;1(11):529-43.

Varghese S. Matrix metalloproteinases and their inhibitors in bone: an overview of regulation and functions. Front Biosci. 2006;1(11):2949-66.

Morel L. Mouse Models of human autoimmune diseases: essential tools that require the proper controls. PLoS Biol. 2004;2(8):e241.

Schmidt RE, Gessner JE. Fc receptors and their interaction with complement in autoimmunity. Immunol Lett. 2005;100:56-67.

Nimmerjahn F, Ravetch JV. Fc gamma receptors as regulators of immune responses. Nat Rev Immunol. 2008;8:34-47.

Shushakova N, Skokowa J, Schulman J, Baumann U, Zwirner J, Schmidt RE et al. C5a anaphylatoxin is a major regulator of activating versus inhibitory FcgammaRs in immune complex-induced lung disease. J Clin Invest. 2002;110:1823-30.

Agarwal V, Malaviya AN. Cytokine network and its manipulation in rheumatoid arthritis. J Indian Rheumatol Assoc. 2005;13:86-91.

Jager DW, Bourcier K, Rijkers TG, Prakken JB, Margolis VS. Prerequisites for cytokine measurements in clinical trials with multiplex immunoassays. BMC Immunol. 2009;10:52.

Chatenoud L. Immune therapies of autoimmune diseases: are we approaching a real cure? Curr Opini Immunol 2006;18(6):710-7.