Rearrangement of antigen receptor genes is defective in mice with severe combined immune deficiency

摘要: A process unique to lymphocyte differentiation is the rearrangement of genes encoding antigen-specific receptors on B and T cells. mouse mutant (C.B-17scid) with severe combined immune deficiency, i.e., that lacks functional cells, shows no evidence such gene rearrangements. However, rearrangements were detected in Abelson murine leukemia virus-transformed bone marrow cells spontaneous thymic lymphomas from C.B-17scid mice. Most these abnormal: approximately 80% Igh deleted entire Jh region, 60% TCR beta J 2 region. The deletions appeared result faulty D-to-J recombination. No abnormal transformed tissues control scid mutation may adversely affect recombinase system catalyzing assembly antigen receptor developing lymphocytes.