Rise in Inulin-Sensitive B Cells During Ontogeny Can Be Prematurely Stimulated by Thymus-Dependent and Thymus-Independent Antigens

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We have shown that the delayed acquisition of competence in expression of an anti-inulin (IN) response by neonatal BALB/c mice is preceded by a natural increase in the frequency of IN-sensitive B cells between 3 to 5 weeks of life. Up until 3 weeks of age, BALB/c mice resemble adult germfree mice in their low frequency of IN-sensitive B cells (1 to 2/106 B cells). Thereafter, the population of IN-reactive B cells rises about 10-fold to the young adult level, without deliberate immunization. This naturally expanded population of IN-reactive cells has an isotype profile resembling populations arising after intentional priming with other antigens in that it contained a large proportion of cells which generated clones expressing immunoglobulin G and immunoglobulin A isotypes, often without detectable immunoglobulin M. The late rise in frequency of IN-sensitive precursors could be induced prematurely by deliberate priming at 3 days of age with either the thymus-dependent antigen IN-hemocyanin or the thymus-independent bacterial levan. However, no circulating anti-IN could be detected following this early administration of antigen. Thus, the delayed expression of anti-IN does not reflect an absence of B cells of the appropriate specificity which can be stimulated to divide by antigen but rather other events occurring subsequent to perinatal generation of antigen-sensitive cells. Our observations support a role for the β2 → 1 fructosyl group as an environmental determinant which selectively expands out preexisting antigen-sensitive B cells at 3 to 5 weeks of age and these include clonotypes which express the predominant anti-IN idiotypes.

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