The intravenous injection of F1 hybrid mice with parental T cells result in a loss in the ability of the F1 mice to generate T-cell mediated immune responses in vitro to graft-versus-host immune deficiency (GVHID). Recognition of host class II MHC antigens by donor cells is required to initiate GVHID. Recognition of host class I MHC antigens may or may not induce GVHID, depending on the class I determinants required. Recognition of class II only abrogates L3T4+ T helper cell responses but not Lyt2+ T helper cell responses; recognition of class I and II results in loss of both L3T4+ and Lyt2+ T helper cell responses. Induction of GVHID by class I and II recognition requires both L3T4+ and Lyt2+ cells; induction of GVHID by class II only recognition requires only L3T4+ parental T cells. GVHID is accompanied by loss of ability to produce IL 2 and in loss of expression of IL 2 receptors. This IL 2 loss was observed in both class I and II and only to a limited extent in class II only GVHID. Recovery of immune function from GVHID was preceeded by recovery of IL 2 receptor expression and IL 2 production. GVHID was used to abrogate natural resistance to bone marrow grafts in Fl hybrid mice, and recognition of host only class II antigens is required to abrogate natural resistance. GVH can also induce immune deficiency in more primitative elements of the lymphohematopoietic system, including thymus and bone marrow functions.
