Although accumulating studies have demonstrated the importance of other co-stimulatory systems in antibody production during conventional immune responses, relatively few have directly addressed their roles in autoreactive T-B interactions. For example, CD137 (4-1BB) antibodies inhibit autoantibody production in both MRL/lpr and (NZBxNZW) F1 lupus-prone mice [58, 59], as well as in graft-versus-host disease models , but may exert an indirect effect via CD8 cells, rather than upon the interaction between helper T cells and autoreac-tive B cells. In addition, several studies have demonstrated abnormal expression of CD134 (0X40 ligand) in SLE  and MG , as well as of CD30 in SLE , autoimmune thyroid disease , systemic sclerosis , pemphigoid , and primary biliary cirrhosis . Other studies have suggested both inhibitory and costimulatory functions for tumor necrosis factor-related apoptosis-induc-ing ligand (TRAIL) [68, 69], and PD-1 deficiency can cause a lupus-like arthritis and glomerulonephritis, as well as an autoantibody-mediated cardiomyopathy [70, 71]. Thus, multiple additional costimulatory systems may modulate the interactions between T and B cells, possibly in both protective and pathogenic fashions.
92 5 T-B Cell Interactions in Autoimmunity 5.2.4
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