Abstract
Abstract For obtaining direct evidence of cellular defects in immunologically deficient chimeras, spleen adherent (A) and nonadherent (T and B) cells, were cultured in vitro with sheep erythrocytes and the plaque-forming cell (PFC) response was determined. Chimera A cells cultured with normal host or donor T and B cells produced normal levels of PFC. The response of chimera T and B cells cultured with normal A cells was considerably lower than that of normal host or donor cells. The response of spleen T and B cells from the allogeneic combination (BALB/c × DBA/2)F1 bone marrow → (C3H × C57BL)F1 was enhanced by thymus cells from rats, normal hosts, and various mouse strains including parental BABL/c (donor) mice but not by cells from normal donors and parental DBA/2 (donor) mice. Bone marrow cells were also ineffective. In the allogeneic combination (C3H × C57BL)F1 → (BALB/c × DBA/2)F1 host thymus again was effective but not donor thymus. Thymus cells from chimeras did not improve the response of either allogeneic combination. Chimera T and B cells cultured with normal host or donor T and B cells severely inhibited the response of host cells but only slightly affected donor cells. Thus, the T cell population is defective in allogeneic chimeras while A cells behave normally and B cells are present and functional in the spleen. Improvement of the response by genetically incompatible (to donor-type chimera cells) thymus cells suggests an allogeneic effect which may be enhanced by the sensitivity of chimera cells to host antigens. The contrasting influences of host, donor, and parental (donor) thymus cells in reconstitution of immune competence indicates that nonspecific and specific factors are operating in inducing immunologic deficiency in chimeras.
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