Regulation of the delayed hypersensitivity reaction in the lung reflected as mononuclear, mast cell and mucus cell appearance after T helper cell depletion and adoptive transfer.
Epicutaneous sensitization with picrylchloride (PiCl) induced a strongly delayed hypersensitivity (DH) reaction in mice. Local challenge in the airways of these mice resulted in increased numbers of mononuclear cells, mast cells and mucus cells. Depletion of T helper cells in vivo by treatment with monoclonal antibody (GK 1.5) inhibited the DH reaction. This treatment also resulted in a decrease in the number of mononuclear and mucus cells in the lung after intranasal challenge. The DH reaction was transferred to recipients with immune lymph node cells and spleen cells from mice sensitized epicutaneously with PiCl. The recipient mice also showed a slight increase in the number of mononuclear cells in the lung after intranasal challenge. These results indicate that T cells are not only involved in the DH reaction but also in the accompanying lung reaction.
D000818:Animals; D004342:Drug Hypersensitivity / Q000209:etiology / Q000473:pathology*; D005260:Female; D006968:Hypersensitivity, Delayed / Q000139:chemically induced / Q000473:pathology*; D007116:Immunization, Passive; D008168:Lung / Q000473:pathology*; D008212:Lymphocyte Depletion; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000473:pathology; D009092:Mucous Membrane / Q000473:pathology; D010853:Picryl Chloride / Q000276:immunology* / Q000633:toxicity; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
D010853:Picryl Chloride