The differential ability of splenic adherent cells from B6.lpr mice to induce suppressor T cells.
Hapten-coupled splenic adherent cells or resident peritoneal cells from autoimmune B6.lpr mice that are over 5 mo of age fail to induce first-order inducer suppressor T cells (Ts1). However, the same population of hapten-coupled cells can induce both delayed-type hypersensitivity responses and third-order effector suppressor T cells (Ts3). Thus, splenic and peritoneal antigen-presenting cells from B6.lpr mice display a defined defect in the ability to induce certain suppressor T cell responses. The cellular defect in Ts1 induction is controlled by the lpr gene, since age-matched congenic B6 mice do not display this defect. The splenic adherent cell defect is temporarily correlated with the autoimmunity that develops in B6.lpr animals. The antigen-presenting defect in the B6.lpr splenic adherent population for Ts1 induction is reversible by culturing the cells in interferon-gamma. The results are discussed as an illustration of the relationship between experimental models of autoimmunity and defects in a suppressor T cell cascade.
D000375:Aging; D000818:Animals; D000938:Antigen-Presenting Cells / Q000145:classification / Q000276:immunology* / Q000502:physiology; D002448:Cell Adhesion; D002478:Cells, Cultured; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007371:Interferon-gamma / Q000494:pharmacology; D007700:Kinetics; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009596:Nitrophenols / Q000276:immunology; D010648:Phenylacetates; D013154:Spleen / Q000166:cytology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D009596:Nitrophenols; D010648:Phenylacetates; C026242:4-hydroxy-5-nitrophenyl acetic acid; D007371:Interferon-gamma