Answers are grounded in this paper and cite their sources.
Trinitrophenyl (TNP)-couple 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 response, 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 o 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.
No takes yet. Share an insight, caveat, or question.
Ikezawa et al. (1981) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: