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Cell Surface Expression of I‐A Products Is Required for Contact Sensitivity Induction by Trinitrophenyl‐Coupled Epidermal Cells
Author(s) -
Ikezawa Zenro,
Sato Masahiro,
Nagai Ryukichi,
Okuda Kenji
Publication year - 1981
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1981.tb00142.x
Subject(s) - microbiology and biotechnology , major histocompatibility complex , biology , spleen , antigen , immunology , cell , histocompatibility , biochemistry , human leukocyte antigen
Trinitrophenyl (TNP)‐coupled epidermal cells (EC) injected subcutaneously (s.c.) were more capable of inducing contact sensitivity (CS) to 2, 4, 6‐trinitro‐1‐chlorobenzene (TNCB) than similarly substituted spleen cells (TNP‐SC). Furthermore, the intravenous (i.v.) or intraperitoneal (i.p.) injection of TNP‐EC also induced CS responses, whereas the i.v. or i.p. injection of TNP‐SC failed to induce them. Treatment of mice with cyclophosphamide (Cy; 50 mg/kg) or anti I‐J serum allowed animals injected with TNP‐SC i.v. to develop significant CS responses, suggesting that Cy‐sensitive and I‐J positive regulatory cells were involved in the induction of unresponsiveness by the i.v. injection of TNP‐SC. Mapping studies of the major histocompatibility gene complex (MHC) region demonstrated that identity at the I‐A subregion alone between EC donor and recipient mice was sufficient for the induction of CS by TNP‐EC given i.v. Blocking experiments using antisera in the absence of complement indicated that I‐A subregion‐encoded antigens on the surface of TNP‐EC apparently are involved in the induction of CS, and are not simply phenotypic markers on the surface of accessory cells.