Regulation of contact allergy in the B cell--deficient mouse.
We have examined the obligate role of B cells in the regulation of allergic contact dermatitis. Our model is ACD in mice made B cell deficient by the chronic administration from birth of a goat antisera to mouse IgM. The following ACD phenomena are well demonstrated in these mice: (1) acquisition and expression of ACD, (2) spontaneous waning of ACD soon after sensitization, (3) immunological tolerance induced by pretreatment with either parenteral hapten or haptenated spleen cells, (4) immunopotentiation by means of either cyclophosphamide or the local administration of a suspension of killed C. parvum (P. acnes), (5) the flare-up of previous test sites following the local administration of parenteral allergen, and (6) acquisition and expression of photo-ACD. We conclude that B cell participation is not required for these ACD phenomena, although an optional or subsidiary function for B regulatory cells is not excluded.
D000276:Adjuvants, Immunologic / Q000008:administration & dosage; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D003520:Cyclophosphamide / Q000494:pharmacology; D003877:Dermatitis, Contact / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006041:Goats; D007108:Immune Tolerance; D007153:Immunologic Deficiency Syndromes / Q000276:immunology / Q000473:pathology; D007249:Inflammation / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D011425:Propionibacterium acnes / Q000276:immunology
D000276:Adjuvants, Immunologic; D003520:Cyclophosphamide