Prophylactic administration of abatacept (CTLA4-Ig; BMS-188667) prevents disease induction and bone destruction in a rat model of collagen-induced arthritis 英文参考文献.docVIP

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Prophylactic administration of abatacept (CTLA4-Ig; BMS-188667) prevents disease induction and bone destruction in a rat model of collagen-induced arthritis 英文参考文献.doc

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Prophylactic administration of abatacept (CTLA4-Ig; BMS-188667) prevents disease induction and bone destruction in a rat model of collagen-induced arthritis 英文参考文献

Available online /supplements/7/S1 Arthritis Research Therapy Volume 7 Supplement 1, February 2005 Meeting abstracts 25th European Workshop for Rheumatology Research Glasgow, UK 24–27 February 2005 Received: 11 January 2005 Published: 17 February 2005 ? 2005 BioMed Central Ltd Speaker abstracts S1 Stem cells now and in the future in medicine A Smith MRC Centre Development in Stem Cell Biology, Institute for Stem Cell Research, University of Edinburgh, UK Arthritis Res Ther 2005, 7(Suppl 1):S1 (DOI 10.1186/ar1506) S3 Autoimmune diabetes: mechanisms A Cooke University of Cambridge, UK Arthritis Res Ther 2005, 7(Suppl 1):S3 (DOI 10.1186/ar1508) Type 1 diabetes is an autoimmune disease that is increasing dramatically in inci- dence in the developed world. Explanations for this increase in incidence include viral precipitation of disease and the so-called ‘hygiene hypothesis’. Abstract not submitted. In Type 1 diabetes the insulin-producing beta cells of the pancreas are selectively destroyed by the immune system. Type 1 diabetes is generally recognised as a T- cell-mediated autoimmune disease with the autoantibody response to islet anti- gens serving as markers of ongoing beta cell destruction. S2 Chaperonins and the regulation of immunity GS Panayi, VC Corrigall Academic Department of Rheumatology, King’s College London, Guy’s Hospital, London, UK Studies in spontaneous animal models of this human condition suggest that it is a Th1-mediated autoimmune disease with an involvement of both CD8+ T cells and macrophages in pathology. There are multiple ways in which the beta cell could be destroyed including a Class I restricted killing by CD8+ T cells, proinflamma- tory cytokine-mediated cell death and death induced by Fas/FasL interactions. At the time of clinical diagnosis it is possible that the patient will have destroyed 70% of their beta cell mass and exogenous insulin is required to maintain glucose home- ostasis. There is currently much interes