Natural killer cells recognize friend retrovirus-infected erythroid progenitor cells through NKG2D-RAE-1 interactions In Vivo.

Natural killer (NK) cells function as early effector cells in the innate immune defense against viral infections and also participate in the regulation of normal and malignant hematopoiesis. NK cell activities have been associated with early clearance of viremia in experimental simian immunodeficiency virus and clinical human immunodeficiency virus type 1 (HIV-1) infections. We have previously shown that NK cells function as major cytotoxic effector cells in vaccine-induced immune protection against Friend virus (FV)-induced leukemia, and NK cell depletion totally abrogates the above protective immunity.

Peptide-induced immune protection of CD8+ T cell-deficient mice against Friend retrovirus-induced disease.

CD8+ CTLs and virus-neutralizing antibodies have been associated with spontaneous and vaccine-induced immune control of retroviral infections. We previously showed that a single immunization with an env gene-encoded CD4+ T cell epitope protected mice against fatal Friend retrovirus infection. Here, we analyzed immune cell components required for the peptide-induced anti-retroviral protection.

Both T and non-T cells with proliferating potentials are effective in inducing suppression of allograft responses by alloantigen-specific intravenous presensitization combined with suboptimal doses of 15-deoxyspergualin.

In an MHC class I-disparate combination of mouse strains, a single intravenous injection of donor spleen cells combined with 10 suboptimal doses of 15-deoxyspergualin (DSG) administration was effective in inducing donor-specific suppression of cytotoxic T-lymphocyte (CTL) responses and prolonged survival of the relevant skin allograft. Proliferative potentials of the donor spleen cells were requirement for the induction of suppressed allospecific responses, but both highly purified T cells and non-T cells were equally effective to induce the suppression of CTL responses by intravenous injection. These results have shown that, although working on different mechanisms, DSG is as effective as FK506 or rapamycin in inducing allograft tolerance when used at suboptimal doses along with the donor-specific intravenous presensitization, and an immune mechanism other than well-characterized veto T cells is working in this model in suppressing alloreactive CTL precursors.