作者: Stephan A. Grupp , Abul K. Abbas , Ming Jiang , Frank E. Cronin
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摘要: There is good evidence for a signaling role played by Ig heavy chain in the developmental transition through pre-B cell stage. We have previously described signal-capable or signal-incapable mutants of μ which defect caused failure to associate with Igα/β heterodimer. To further characterize chain-mediated vivo, as well B development and allelic exclusion, we created transgenic mice cells express these mutant chains. Failure signal via results block expressing μ. A small number animals do escape are expressed spleen periphery B220 + IgM cells. These respond LPS proliferating but show no response T-independent-specific Ag. In contrast, receptor strong Ag-specific stimulus. Igα seen association signal-deficient IgM. Thus, complex not assembled, can be delivered. Despite signaling, exclusion complete. detectable coexpression endogenous murine IgM, nor there rearrangement genes. This suggests that differing mechanisms responsible thus allows separate examination mechanisms.