Mononuclear cells from human lung parenchyma support antigen-induced T lymphocyte proliferation

L. P. Nicod, M. F. Lipscomb, J. C. Weissler, G. B. Toews

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

We have previously demonstrated that there is a subpopulation of loosely adherent pulmonary mononuclear cells that can be isolated from minced and enzyme-digested lung tissue with a potent capacity to stimulate allogeneic T lymphocyte proliferation. We now demonstrate that these cells are also capable of stimulating an autologous mixed leukocyte reaction (AMLR) and presenting antigen to autologous T lymphocytes. These loosely adherent mononuclear cells (LAM) were more effective than either alveolar macrophages or monocytes as antigen-presenting cells. Depletion of phagocytic or Fc receptor-positive cells from the LAM population enhanced the stimulation of a reaction AMLR while preserving antigen-induced T lymphocyte proliferation. These results indicate that there are nonphagocytic, Fc receptor-negative accessory cells in human lung parenchyma capable of activating resting T cells in an AMLR and supporting antigen-specific T lymphocyte proliferation. The identity of these cells is uncertain, but the data strongly suggest that the cell is not a classical monocyte-derived macrophage. These antigen-presenting cells may be critical in the initiation of immune responses within the lung.

Original languageEnglish (US)
Pages (from-to)336-344
Number of pages9
JournalJournal of Leukocyte Biology
Volume45
Issue number4
StatePublished - 1989

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T-Lymphocytes
Antigens
Lung
Mixed Lymphocyte Culture Test
Fc Receptors
Antigen-Presenting Cells
Autoantigens
Alveolar Macrophages
Monocytes
Macrophages
Enzymes
Population

ASJC Scopus subject areas

  • Cell Biology

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Mononuclear cells from human lung parenchyma support antigen-induced T lymphocyte proliferation. / Nicod, L. P.; Lipscomb, M. F.; Weissler, J. C.; Toews, G. B.

In: Journal of Leukocyte Biology, Vol. 45, No. 4, 1989, p. 336-344.

Research output: Contribution to journalArticle

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