Induction of cell-mediated cytotoxic self responses by epidermal cells modified with a haptenic sulphydryl reagent

H. Pehamberger, Robert B Levy, P. Henkart, S. I. Katz

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Abstract

Murine epidermal cells (EC) act as stimulator cells in the generation of allogeneic cytotoxic T lymphocytes (CTL) in cell-mediated lympholysis (CML) and are suitable targets for allogeneic and hapten-self CTL. To analyse the role of EC in the generation of and recognition by anti-self CTL, syngeneic hapten-modified murine EC were used as in vivo and in vitro stimulating populations and as target cells in a hapten-self CML system. Epidermal cells were modified with the sulphydryl-reactive haptenic reagent N-iodoacetyl-N'-(5-sulphonic-1-naphthyl)ethylenediamine (I-AED). C3H.SW (H-2(b)) AED-self CTL responses were generated by stimulation with syngeneic AED-modified EC and were readily demonstrated when tested on syngeneic hapten-modified EC. These CML responses were hapten-specific and H-2-restricted. No substantial difference was detected in the ability of AED-modified EC and spleen cells (SC) to stimulate the generation of secondary AED-self CTL. Cold target inhibition experiments with hapten-modified EC and SC blockers did not reveal tissue-specific recognition of hapten-modified EC or SC targets by AED-self CTL. These findings demonstrate that hapten-modified EC, when used for priming in vivo and subsequently for in vitro sensitization, can induce hapten-specific self CTL that are reactive against syngeneic hapten-modified EC.

Original languageEnglish
Pages (from-to)333-341
Number of pages9
JournalScandinavian Journal of Immunology
Volume16
Issue number4
StatePublished - Jan 1 1982
Externally publishedYes

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Haptens
Cytotoxic T-Lymphocytes
ethylenediamine
Spleen
Health Services Needs and Demand

ASJC Scopus subject areas

  • Immunology

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Induction of cell-mediated cytotoxic self responses by epidermal cells modified with a haptenic sulphydryl reagent. / Pehamberger, H.; Levy, Robert B; Henkart, P.; Katz, S. I.

In: Scandinavian Journal of Immunology, Vol. 16, No. 4, 01.01.1982, p. 333-341.

Research output: Contribution to journalArticle

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