Rheumatoid Arthritis: Pernis AB

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A digest of articles written 1999 and later, on the topic "Arthritis, Rheumatoid," originating from Planet Earth —» Pernis AB.  Display:  All Citations ·  All Abstracts
1 Review Th17 cells in rheumatoid arthritis and systemic lupus erythematosus. 2009

Pernis AB. · Department of Medicine, Columbia University, New York, NY 10032, USA. · J Intern Med. · Pubmed #19493058 No free full text.

Abstract: Recent work has implicated a novel Th effector cell subset, the Th17 cell subset, in the development of both rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) because of the ability of Th17 cells to produce cytokines like IL-17 and IL-21 that can drive both inflammatory and humoral responses. In this review, we will discuss recent studies that have begun elucidating the factors that regulate the development of Th17 cells and provide a brief overview of the role of Th17 cells in RA and SLE.

2 Article IRF-4-binding protein inhibits interleukin-17 and interleukin-21 production by controlling the activity of IRF-4 transcription factor. 2008

Chen Q, Yang W, Gupta S, Biswas P, Smith P, Bhagat G, Pernis AB. · Department of Medicine, Columbia University, New York, NY 10032, USA. · Immunity. · Pubmed #19062315 No free full text.

Abstract: The T helper 17 (Th17) cell lineage is important in inflammatory and autoimmune responses, via its ability to produce interleukin-17 (IL-17) and IL-21. Given the potentially deleterious effects of Th17 cells, their generation needs to be strictly controlled. IRF-4 is a transcription factor that has recently emerged as a key regulator of Th17 cell differentiation. Here, we showed that mice deficient in a previously isolated protein, IBP (IRF-4-binding protein), rapidly developed rheumatoid arthritis-like joint disease and large-vessel vasculitis. The pathology was associated with an enhanced responsiveness of T cells to low levels of stimulation and with the inappropriate synthesis of IL-17 and IL-21. IBP sequestered IRF-4 and prevented it from targeting the transcriptional regulatory regions of the genes that encode IL-17 and IL-21. Thus, IBP appears to be important in preventing T cell-mediated autoimmunity by ensuring that the production of IL-17 and IL-21 does not occur in response to self-antigens.