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To detect the potential role of collagen type II immune complexes in granulocyte activation and acute inflammatory arthritis

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To detect the potential role of collagen type II immune complexes in granulocyte activation and acute inflammatory arthritis

Rheumatoid Arthritis (RA) is an autoimmune disease characterized by symptoms like joint pain, inflammation and cartilage damage. Major component of joint cartilages is collagen type II (CII). Antibodies against CII (anti-CII antibodies) are found in serum of a subgroup of patients with RA. Anti-CII antibodies form immune complexes (IC) with collagen II present in the joint cartilage. Specific group of patients with high levels of anti-CII antibody containing IC (anti-CII IC) have an acute onset showing early joint erosions and inflammation. Innate immune cells like monocytes and granulocytes are found in high numbers in areas of joint inflammation. Previous studies in our group have shown that anti-CII IC stimulate peripheral blood mononuclear cells (PBMC) isolated from human blood to produce cytokines measured by laboratory technique, cytokine enzyme linked immunosorbent assay (cELISA). When the monocytes were depleted from the PBMC the effect of cytokine production was diminished significantly showing that monocytes are primarily responsible for the cytokine production. Hence it is interesting to find the impact of anti-CII IC in granulocytes isolated from healthy blood donors by various laboratory analytical techniques like flow cytometry, measurement of toxic radicals released by granulocytes stimulated with anti-CII IC and measurement of cytokines produced by granulocytes stimulated by anti-CII IC.

VIVEK ANAND MANIVEL

Master programme in Applied Biotechnology

Master thesis in Applied Biotechnology, 45 hp, 2011-12

Department of Immunology, Genetics and Pathology (IGP), Rudbeck laboratory, Uppsala University

Supervisor: Associate Professor Johan Rönnelid, M.D, PhD.

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