Mechanisms underlying generation and activation of class II MHC-restricted B lymphocytes and their function

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1. I-A molecules serve as restriction elements of the class 11 major histocompatibility complex (MHC) -restricted B-B cell interaction involved in the polyclonal B cell differentiation, but I-E molecules do not exhibit such activity. Moreover, cross-linking by anti-I-E mAb of I-E molecules on B cells induces increases in intracellular CAMP levels, whereas such increases are not elicited by cross-linking of I-A molecules, indicating disparate function of I-A and I-E molecules expressed on B cells.2. The B lymphoma cells expressing relevant I-A molecules function as auxiliary cells in the class II MHC-restricted B cell activation, While neither I-A-positive macrophage lines nor I-A-transfected fibroblasts collaborate with class II NMC-restricted B cells. Thus, B-cell unique signals play a critical role in the B-cell activation.3. It is shown that there exist at least two distinct mechanisms in the T-independent B cell activation pathway. Anti-trinitrophenyl (TNP) antibody responses induced by LPS require class 11 MHC-restricted B-B cell inter-action but not surface Ig-mediated signaling, whereas those evoked by TNP-LPS con ugates are dependent on signaling through surface Ig but not by class 11 MHC molecules. This implies that signal transduction through surface Ig overcomes the requirement for class 11 MHC-mediated signaling.4. In the anti-BrMRBC (bromelain-treated mouse red blood cell) autoantibody responses induced by LPS, genotypically low-responder B cells are converted to highresponder phenotype if the low-responder B cells mature under the conditions in which they are able to acquire the restriction specificity for high-responder type of class 11 MHC molecules.