Studies of the role of mast cells in contact sensitivity responses. Passive transfer of the reaction into mast cell-deficient mice locally reconstituted with cultured mast cells: Effect of reserpine on transfer of the reaction with DNP-specific cloned T cells

Yoseph A. Mekori, Jennie C C Chang, Barry K. Wershil, Stephen J. Galli*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

The role of mast cells in the elicitation of contact sensitivity (CS) responses was evaluated by transferring different aliquots of the same preparations of immune lymph node cells (I-LNC) into naive, genetically mast cell-deficient (WBB6F1-W/Wv or WCB6F1-S1/S1d) mice and the corresponding congenic normal (+/+) mice. We found that the 24-hr CS responses elicited in the recipient mast cell-deficient mice were statistically indistinguishable from those in the congenic +/+ mice according to four different criteria: micrometer measurements of ear swelling, ratios of the weight or [125I]iododeoxyuridine-labeled leukocyte infiltration-associated cpm in challenged and contralateral control ears, and amount of 125I-fibrin deposition. We also transferred I-LNC into WBB6F1-W/Wv mice which, 5 months earlier, had undergone local repair of their mast cell deficiency by the intradermal injection (into the left ear only) of growth factor-dependent cultured mast cells derived from congenic +/+ mice. When 24-hr CS responses were elicited in both ears of these mice, the reactions in the mast cell-reconstituted left ears were similar to those in the mast cell-deficient right ears. We also found that treatment of antigen-specific cloned T cells with reserpine in vitro markedly impaired their ability to transfer reactivity for CS, providing further evidence that reserpine can interfere with the expression of T-cell-mediated responses through effects independent of its action on mast cells.

Original languageEnglish (US)
Pages (from-to)39-52
Number of pages14
JournalCellular Immunology
Volume109
Issue number1
DOIs
StatePublished - Oct 1 1987

Funding

’ Supported by U.S. Public Health Service Research Grants AI 20292, AI 22674, AI 23990, and CA 28834 and Physician-Scientist Award (to B. K. Wershil) KI 1 AM 01543. Y. A. Mekori was supported in part by a fellowship from the Israel Cancer Research Fund. J. C. C. Chang was a Special Fellow of the Leukemia Society of America. * Present address: Department of Medical Microbiology and Immunology, MS 409, University of Kentucky Medical Center, 800 Rose St., Lexington, KY 40536-0084. 3 To whom correspondence should be addresseda t Department of Pathology, Beth Israel Hospital, 330 Brookline Ave., Boston, MA 022 15.

ASJC Scopus subject areas

  • Immunology

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