Abstract

Abstract The primary thymus-dependent IgG anti-sheep red blood cell (SRBC) response of (CBA/N × DBA/2)F1 male mice was <10% of that of immunologically normal (CBA/N × DBA/2)F1 female mice. Adoptive transfers of activated T cells (ATC) and either bone marrow or anti-ϑ-treated spleen cells from F1 mice into lethally irradiated recipients demonstrated that the functional helper-cell activity of ATC from immune-defective and normal F1 mice was equivalent. By contrast, B lymphocytes of (CBA/N × DBA/2)F1 male mice gave very poor or absent IgG anti-SRBC responses in this system, whereas the response of B cells from immunologically normal F1 mice was excellent. The poor response of (CBA/N × DBA/2)F1 male B cells was not improved by providing additional T cell help, suggesting that these cells were refractory to a large proportion of this help. Furthermore, increasing the number of donor B cells from immune-defective mice failed to influence materially the IgG anti-SRBC response. Although the response of (CBA/N × DBA/2)F1 male primed B cells was considerably improved over that of unprimed cells, it remained less than the primary response of immunologically normal F1 mice. The presence of a low but detectable SRBC response in (CBA/N × DBA/2)F1 male mice suggests that the B cells of these mice, and by inference those of normal mice, can be triggered by antigen in the presence of ATC through a mechanism that is independent of Lyb 3+, 5+ B cells. The large increase in the response of (CBA/N × DBA/2)F1 male B cells to SRBC after priming suggests that Lyb 3+, 5+ B cells are not necessary for the generation of memory B cells. An interesting difference in the environments of (CBA/N × DBA/2)F1 vs (DBA/2 × CBA/N)F1 male mice was demonstrated by reconstituting these mice with mixtures of ATC and B cells after lethal irradiation. In all cases, the IgG responses of the immune-defective F1 mice were significantly less than those of the immunologically normal mice. Mechanisms that could explain these findings are discussed.

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