Surface markers, heavy chain sequences and B cell lineages.
A unifying theory of B cell development and lineage commitment is presented. There are two firmly established B lineages: cells which normally arise only from fetal sources and lack N insertions in their rearranged heavy chains; and N-containing cells which arise from adult bone marrow precursors (and perhaps from late fetal sources). Commitment to the expression of CD5 and the capacity for long-life (or self-renewal) are induced as a consequence of sIg cross-linking, typically by a repeating epitope, thymus independent type two antigen. Alternatively, activation resulting from cognate interaction with a helper T cell does not induce CD5 but results in lower expression of J11d. In this case activation occurs in the absence of sIg cross-linking. It is further proposed that differences in the Ig repertoire make it highly likely that fetal/neonatal, but not adult derived B cells will be induced to express CD5. The model offers a plausible explanation for the correlation of CD5 expression and natural autoantibody production by neonatal B cells. Possible sources of pathogenic autoantibody are discussed in the context of this model.
Wortis
H H
HH
Department of Pathology, Tufts University School of Medicine, Boston, MA.
D000818:Animals; D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D018956:CD5 Antigens; D015326:Gene Rearrangement, B-Lymphocyte, Heavy Chain; D005803:Genes, Immunoglobulin; D006801:Humans; D008213:Lymphocyte Activation; D051379:Mice; D008954:Models, Biological
D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D018956:CD5 Antigens