Divergent Tγ cell functions in antigen-induced blastogenesis: facilitory interactions with Tnonγ cells and participation in monocyte- and prostaglandin-mediated suppression

Mary Ellen Kleinhenz, Jerrold J. Ellner

Research output: Contribution to journalArticle

Abstract

The contribution of Tγ cells, i.e., T cells bearing surface receptors for the Fc portion of IgG, to the immunologic response to antigen has not been assessed in health or disease. We examined the role of Tγ cells in antigen-induced blastogenesis of T cells from healthy subjects and characterized their participation in monocyte- and prostaglandin-mediated suppression. Cell fractions enriched in and depleted of Tγ cells were prepared from nonadherent T cells by preparative resetting with IgG-sensitized ox erythrocytes; antigen-induced blastogenesis was assayed as 3H-thymidine incorporation (3H-TdR), by microculture techniques. Removal of Tγ cells resulted in a Tnonγ cell fraction whose in vitro response to soluble antigen was a mean 40% ± 8 less than the response of the unseparated T cells from the same donors. Antigen did not induce 3H-TdR in cultures of Tγ cells; however, in cell-mixing experiments, addition of autologous Tγ cells reconstituted the antigen responsiveness of the Tnonγ cell fraction. Monocytes (MN) added to cell cultures at a ratio known to be suppressive in vitro (MN to T = 1:4) significantly decreased antigen-induced 3H-TdR of unseparated T cells but did not alter the antigen responses of Tnonγ cells. MN-dependent suppression was abrogated by co-culture with indomethacin. Exogenous prostaglandin E2, an immunosuppressive cyclooxygenase product of MN, selectively decreased antigen-induced 3H-TdR of cell cultures containing Tγ cells but did not affect antigen responses of Tnonγ cell fraction. Thus these studies show that MN and their cyclooxygenase products modulate Tγ cells to function in a suppressive mode. This demonstration of divergent Tγ cell functions indicates that the contribution of an expanded Tγ cell population to altered antigen reactivity in disease can be determined only by careful functional studies.

Original languageEnglish (US)
Pages (from-to)751-761
Number of pages11
JournalThe Journal of Laboratory and Clinical Medicine
Volume102
Issue number5
StatePublished - 1983
Externally publishedYes

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T-cells
Lymphocyte Activation
Prostaglandins
Monocytes
T-Lymphocytes
Antigens
Thymidine
Cell culture
Prostaglandin-Endoperoxide Synthases
Bearings (structural)
Cell Culture Techniques
Immunoglobulin G
Fc Receptors
Cell Surface Receptors
Immunosuppressive Agents
Coculture Techniques
Dinoprostone
Indomethacin

ASJC Scopus subject areas

  • Medicine(all)
  • Pathology and Forensic Medicine

Cite this

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title = "Divergent Tγ cell functions in antigen-induced blastogenesis: facilitory interactions with Tnonγ cells and participation in monocyte- and prostaglandin-mediated suppression",
abstract = "The contribution of Tγ cells, i.e., T cells bearing surface receptors for the Fc portion of IgG, to the immunologic response to antigen has not been assessed in health or disease. We examined the role of Tγ cells in antigen-induced blastogenesis of T cells from healthy subjects and characterized their participation in monocyte- and prostaglandin-mediated suppression. Cell fractions enriched in and depleted of Tγ cells were prepared from nonadherent T cells by preparative resetting with IgG-sensitized ox erythrocytes; antigen-induced blastogenesis was assayed as 3H-thymidine incorporation (3H-TdR), by microculture techniques. Removal of Tγ cells resulted in a Tnonγ cell fraction whose in vitro response to soluble antigen was a mean 40{\%} ± 8 less than the response of the unseparated T cells from the same donors. Antigen did not induce 3H-TdR in cultures of Tγ cells; however, in cell-mixing experiments, addition of autologous Tγ cells reconstituted the antigen responsiveness of the Tnonγ cell fraction. Monocytes (MN) added to cell cultures at a ratio known to be suppressive in vitro (MN to T = 1:4) significantly decreased antigen-induced 3H-TdR of unseparated T cells but did not alter the antigen responses of Tnonγ cells. MN-dependent suppression was abrogated by co-culture with indomethacin. Exogenous prostaglandin E2, an immunosuppressive cyclooxygenase product of MN, selectively decreased antigen-induced 3H-TdR of cell cultures containing Tγ cells but did not affect antigen responses of Tnonγ cell fraction. Thus these studies show that MN and their cyclooxygenase products modulate Tγ cells to function in a suppressive mode. This demonstration of divergent Tγ cell functions indicates that the contribution of an expanded Tγ cell population to altered antigen reactivity in disease can be determined only by careful functional studies.",
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PY - 1983

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N2 - The contribution of Tγ cells, i.e., T cells bearing surface receptors for the Fc portion of IgG, to the immunologic response to antigen has not been assessed in health or disease. We examined the role of Tγ cells in antigen-induced blastogenesis of T cells from healthy subjects and characterized their participation in monocyte- and prostaglandin-mediated suppression. Cell fractions enriched in and depleted of Tγ cells were prepared from nonadherent T cells by preparative resetting with IgG-sensitized ox erythrocytes; antigen-induced blastogenesis was assayed as 3H-thymidine incorporation (3H-TdR), by microculture techniques. Removal of Tγ cells resulted in a Tnonγ cell fraction whose in vitro response to soluble antigen was a mean 40% ± 8 less than the response of the unseparated T cells from the same donors. Antigen did not induce 3H-TdR in cultures of Tγ cells; however, in cell-mixing experiments, addition of autologous Tγ cells reconstituted the antigen responsiveness of the Tnonγ cell fraction. Monocytes (MN) added to cell cultures at a ratio known to be suppressive in vitro (MN to T = 1:4) significantly decreased antigen-induced 3H-TdR of unseparated T cells but did not alter the antigen responses of Tnonγ cells. MN-dependent suppression was abrogated by co-culture with indomethacin. Exogenous prostaglandin E2, an immunosuppressive cyclooxygenase product of MN, selectively decreased antigen-induced 3H-TdR of cell cultures containing Tγ cells but did not affect antigen responses of Tnonγ cell fraction. Thus these studies show that MN and their cyclooxygenase products modulate Tγ cells to function in a suppressive mode. This demonstration of divergent Tγ cell functions indicates that the contribution of an expanded Tγ cell population to altered antigen reactivity in disease can be determined only by careful functional studies.

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