Abstract

CBA/N mice have an X-linked immunodeficiency that includes a deficient humoral response to sheep red blood cells (SRBC). In order to study the cellular mechanisms of this deficiency we have examined helper T cell function to SRBC in an adoptive transfer system by using 2 different sources of helper T cells. When thymocytes were used as the source of helper T cell precursors in an adoptive transfer system, CBA/N thymocytes were as effective as CBA/Ca thymocytes in inducing CBA/Ca bone marrow cells to develop into both direct and indirect anti-SRBC plaque-forming cells (PFC). However, when SRBC-primed, irradiated recipient mice were used as the source of helper T cells, primed and irradiated CBA/N recipients developed significantly fewer direct and indirect anti-SRBC PFC than similarly treated CBA/Ca recipients when reconstituted with CBA/Ca bone marrow cells and challenged with SRBC. This difference in radioresistant helper T cell function was also observed when primed, irradiated (CBA/N X DBA/2)F1 defective male and nondefective female mice were used as recipients of F1 female bone marrow cells and SRBC, confirming that this defect is a part of the X-linked CBA/N immunodeficiency. This deficiency in radioresistant helper T cell function in CBA/N mice does not appear to be due either to suppressor T cell function, or to a negative effect of the CBA/N environment on either B cell maturation, T cell-B cell cooperation, or helper T cell function. We conclude that antigen-primed helper T cell function in CBA/N mice is radiosensitive. Possible reasons for this are evaluated and discussed.

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