Altered allogeneic response in neonatally anti-MHC class I-treated mice.

Neonatal treatment of C3H mice (H-2k) with anti-Kk monoclonal antibodies results in altered cytotoxic responses against allogeneic targets. After 2-3 weeks of antibody treatment, no difference in the number of CD4+8- or CD4-8+ T cells was observed between the antibody- and saline-treated mice. However, antibody-treated mice had a significantly reduced cytotoxic response against various allogeneic major histocompatibility complex (MHC) class I-expressing targets.

Increased number of CD4-CD8+ MHC class II-specific T cells in MHC class II-deficient mice.

Targeted disruption of the A beta-encoding gene of H2b mice abolishes major histocompatibility complex (MHC) class II expression and results in a failure to develop CD4+8- T cells. Besides this major effect, the lack of class II expression affects the level of T-cell receptor (TCR) and CD4 expression on differentiating thymocytes. Moreover, there is no class II-mediated negative selection of thymocytes.

CD4+ and CD8+ alpha beta, and gamma delta T cells are cytotoxic effector cells of beta 2-microglobulin-deficient mice against cells having normal MHC class I expression.

Despite original reports that describe the absence of CD8+ CTLs in mice having homozygous deficiency in the beta 2-microglobulin gene, strong cytotoxic activities against cells with normal beta 2-microglobulin expression were observed in these animals. This cytotoxicity was reproducibly induced by immunizations with allogeneic or syngeneic cells. MHC class II expression by the stimulator cells was not required.

Increased number of cytotoxic T cells within CD4+8- T cells in beta 2-microglobulin, major histocompatibility complex class I-deficient mice.

Targeted disruption of beta 2-microglobulin gene results in deficient major histocompatibility complex class I expression and failure to develop CD4-8+ T cells. Despite this, beta 2 M-/- mice reject skin grafts and cope with most viral infections tested. We asked whether CD4+8- cytotoxic T cells would play a role in compensating for the defect in CD4-8+ cytotoxic T cell function.

Humoral immune response to the antigen administered as an immune complex.

Antigen (HSA) bound in immune complexes at equivalence with syngeneic anti-HSA antibodies elicit much stronger humoral immune response then soluble HSA. On the other hand, administration of immune complexes formed with xenogeneic (rabbit) anti-HSA antibodies suppressed humoral immune response against HSA, but not against rabbit IgG in mice. We suggest that immunization with antigen bound in immune complex might represent a powerful tool in enhancing humoral immune responses.