Carbohydrate surface constituents of T cells mediating delayed-type hypersensitivity that control entry into sites of antigen deposition.
Peritoneal exudate T lymphocytes (PETLs) that mediate delayed-type hypersensitivity (DTH) to sheep red blood cells in mice were modified by in vitro treatment methods which modify surface carbohydrate constituents. Neuraminidase treatment resulted in the release of both N-acetylneuraminic acid and N-glycolyl-neuraminic acid, and periodate treatment in the formation of the corresponding C7 analogues. Treatment of PETLs with neuraminidase led to a transient reduction of DTH reactions in syngeneic cell recipients. After treatment with neuraminidase plus galactose oxidase, adoptive mediation of DTH was more markedly reduced. Incubation of PETLs with periodate caused a permanent loss of DTH transferring capacity. The oxidation-induced effects following treatment of PETLs with neuraminidase plus galactose oxidase or with periodate could be reversed by subsequent reduction with borohydride of the previously formed aldehyde moieties. Decreased DTH reactions observed after the various treatment procedures were paralleled by reduced immigration of PETLs into sites of antigen deposition, indicating that the reduction/oxidation state of cell surface carbohydrates is crucial for induction of inflammatory processes by T cells. Trapping of PETLs in the liver could not be the sole mechanism since neuraminidase- and periodate-treated PETLs, but not neuraminidase plus galactose oxidase-treated PETLs, accumulated in the liver. It therefore appears that alterations in the reduction/oxidation state of the cell surface can lead to unresponsiveness of T cells to inflammatory signals.
D000818:Animals; D000954:Antigens, Surface / Q000276:immunology*; D002241:Carbohydrates / Q000276:immunology*; D005260:Female; D005692:Galactose Oxidase / Q000494:pharmacology; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D009439:Neuraminidase / Q000494:pharmacology; D010084:Oxidation-Reduction; D010504:Periodic Acid / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D000954:Antigens, Surface; D002241:Carbohydrates; D010504:Periodic Acid; D005692:Galactose Oxidase; D009439:Neuraminidase