title: Genetic control of contact photosensitivity to tetrachlorosalicylanilide. II. Igh complex controls the sensitivity induced by photohapten-modified spleen cells but not epidermal cells.
abstract: We studied the genetic control of murine contact photosensitivity (CPS)1 to 3,3',4',5-tetrachlorosalicylanilide (TCSA) that was induced by subcutaneous injection of TCSA-photomodified epidermal cells (photoTCSA-EC) and spleen cells (photoTCSA-SC). With regard to the H-2 locus, sensitization with both types of photohaptenated cells showed the same pattern of CPS responses: H-2k and H-2b,d haplotypes were closely associated with low and high responders, respectively. On the other hand, the Igh locus affected the CPS reaction induced by photoTCSA-SC but not -EC; the Igh-1d allotype was related to low responsiveness, while high responders possessed Igh-1a,b. Thus, the photoTCSA-SC sensitization was controlled by H-2 and Igh in a codominant manner. The photoTCSA-SC-induced responses of H-2k but not Igh-1d mice were enhanced by CY pretreatment, suggesting that the mechanisms of low responsiveness in H-2k and Igh-1d mice were different. H-2 identity between donors of photoTCSA-EC and recipients was sufficient for effective sensitization, whereas both H-2 and Igh between donors of photoTCSA-SC and recipients should be identical to obtain maximum sensitization. This further confirmed the involvement of the Igh complex in the genetic control of CPS evoked by photoTCSA-SC. B cells as well as macrophages served as an effective presentation template for the photoTCSA-SC sensitization in the high responder Igh-1a mice, whereas B cells failed in inducing the CPS reaction in the low responder Igh-1d mice. These results suggest that B cells play an essential role in the Igh control phenomenon seen in the photoTCSA-SC sensitization. The present study demonstrated that CPS induced by photohapten-modified cells are differentially regulated by the H-2 and Igh gene loci depending on the cell type used for sensitization.
authors.affiliation: Department of Dermatology, Hamamatsu University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Tokura
authors.forename: T
authors.initials: T
authors.lastname: Satoh
authors.forename: M
authors.initials: M
authors.lastname: Yamada
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D003520:Cyclophosphamide / Q000494:pharmacology; D004817:Epidermis / Q000276:immunology*; D005803:Genes, Immunoglobulin; D006183:H-2 Antigens / Q000235:genetics*; D051379:Mice; D008815:Mice, Inbred Strains; D010787:Photosensitivity Disorders / Q000235:genetics*; D012458:Salicylanilides / Q000276:immunology*; D013154:Spleen / Q000276:immunology*
chemical_list: D006183:H-2 Antigens; D012458:Salicylanilides; D003520:Cyclophosphamide; C003390:3,3',4',5-tetrachlorosalicylanilide