By Fleming Pociot
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35. Liang B, Gee RJ, Kashgarian MJ et al. 2 blocking antibodies. J Immunol 1999; 163(4):2322-9. 36. Kaneko H, Saito K, Hashimoto H et al. Preferential elimination of CD28+ T cells in systemic lupus erythematosus (SLE) and the relation with activation-induced apoptosis. Clin Exp Immunol 1996; 106(2):218-29. 37. Garcia-Cozar FJ, Molina IJ, Cuadrado MJ et al. Defective B7 expression on antigen-presenting cells underlying T cell activation abnormalities in systemic lupus erythematosus (SLE) patients.
28 Taken together with the significant CTLA-4 expression on synovial fluid T cells, these findings reflect the increased activation state of T cells in patients with RA and may have important implications for the pathogenesis of the disease. Potential Pathogenetic Role of CTLA-4 in T Cell-Mediated Interactions in RA The possible role of CTLA-4 in the initiation phase of rheumatoid inflammation has not been addressed so far. Whether polymorphic CTLA-4 alleles are associated with impaired CTLA-4 molecule inhibitory function remains to be elucidated.
Scheipers PReiser H. Fas-independent death of activated CD4+ T lymphocytes induced by CTLA-4 crosslinking. Proc Natl Acad Sci USA 1998; 95:10083-10088. 38. Brunner MC, Chambers CA, Chan FK et al. CTLA-4-Mediated inhibition of early events of T cell proliferation. J Immunol 1999; 162:5813-5820. 39. Griffin MD, Hong DK, Holman PO et al. Blockade of T cell activation using a surface-linked single-chain antibody to CTLA-4 (CD152). J Immunol 2000; 164:4433-4442. 40. Linsley PS, Bradshaw J, Greene J et al.
CTLA-4 in Autoimmune Disease (Medical Intelligence Unit (Unnumbered : 2003).) by Fleming Pociot