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Variation in T and B Cell Deficiency in Different Mouse Allogeneic Radiation Chimeras

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Abstract The immunologic deficiency of allogeneic radiation chimeras was examined in vitro by culturing spleen cells of the chimera with allogeneic or syngeneic (to donor-type cells of the chimera) activated thymus-derived (T) cells (ATC) or bone marrow-derived (B) cells. The plaque-forming cell (PFC) response to sheep RBC of spleen cells from 100% of the CD2F1 → C3BF1 chimeras was improved considerably (27-fold) with allogeneic ATC but syngeneic ATC gave only a 2-fold increase. Allogeneic B cells induced a moderate increase (4-fold) in the response of spleen cells from only 19% of the chimeras while syngeneic B cells were ineffective. With spleen cells from the reciprocal C3BF1 → CD2F1 chimera there was only a 7-fold increase in the response with allogeneic ATC in 38% of the chimeras and only a 2- to 3-fold increase in 18% with syngeneic ATC. In contrast, there was a 27-fold increase in PFC in about 45% of these latter chimeras with allogeneic B cells while syngeneic B cells failed to improve the response. The PFC generated in mixtures involving both types of chimera spleen cells cultured together were typed with specific isoantiserum and shown to be of CD2F1 origin. These results demonstrate that deficiency in the interacting cellular components of the spleen will vary in different chimeras. Thus, CD2F1 → C3BF1 chimeras are primarily T cell deficient while those of the reciprocal combinations, C3BF1 → CD2F1, are deficient primarily in the B cell population.
Title: Variation in T and B Cell Deficiency in Different Mouse Allogeneic Radiation Chimeras
Description:
Abstract The immunologic deficiency of allogeneic radiation chimeras was examined in vitro by culturing spleen cells of the chimera with allogeneic or syngeneic (to donor-type cells of the chimera) activated thymus-derived (T) cells (ATC) or bone marrow-derived (B) cells.
The plaque-forming cell (PFC) response to sheep RBC of spleen cells from 100% of the CD2F1 → C3BF1 chimeras was improved considerably (27-fold) with allogeneic ATC but syngeneic ATC gave only a 2-fold increase.
Allogeneic B cells induced a moderate increase (4-fold) in the response of spleen cells from only 19% of the chimeras while syngeneic B cells were ineffective.
With spleen cells from the reciprocal C3BF1 → CD2F1 chimera there was only a 7-fold increase in the response with allogeneic ATC in 38% of the chimeras and only a 2- to 3-fold increase in 18% with syngeneic ATC.
In contrast, there was a 27-fold increase in PFC in about 45% of these latter chimeras with allogeneic B cells while syngeneic B cells failed to improve the response.
The PFC generated in mixtures involving both types of chimera spleen cells cultured together were typed with specific isoantiserum and shown to be of CD2F1 origin.
These results demonstrate that deficiency in the interacting cellular components of the spleen will vary in different chimeras.
Thus, CD2F1 → C3BF1 chimeras are primarily T cell deficient while those of the reciprocal combinations, C3BF1 → CD2F1, are deficient primarily in the B cell population.

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