Human alveolar macrophages inhibit receptor-mediated increases in intracellular calcium concentration in lymphocytes.

W. C. Yarbrough, D. S. Wilkes, J. C. Weissler

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Prior studies have demonstrated that human alveolar macrophages (AM) are suppressive of lymphocyte function, through the mechanism of inhibition is unclear. In the current study, human AM inhibited receptor-mediated increases in intracellular calcium concentration ([Ca2+]i) in T cells, natural killer cells, and B cells. This effect was produced by either live or fixed AM, while peripheral blood monocytes caused a minimal reduction in [Ca2+]i. The inhibitory effect of AM was seen following 1 to 2 h of incubation with lymphocytes, was complete at 16 h, and did not affect ionomycin-mediated [Ca2+]i. Inhibition of [Ca2+]i by AM correlated with suppression of T-lymphocyte proliferation and cytotoxic T-lymphocyte activity in response to alloantigen and Staphylococcus A-induced immunoglobulin production. Our findings suggest that a membrane signal on AM is capable of inhibiting receptor-mediated signal transduction in lymphocytes and that this is likely a major mechanism by which immune responses are downregulated in the alveolus.

Original languageEnglish (US)
Pages (from-to)411-415
Number of pages5
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume5
Issue number5
StatePublished - Nov 1991
Externally publishedYes

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Lymphocytes
Alveolar Macrophages
Calcium
T-cells
T-Lymphocytes
Signal transduction
Ionomycin
Isoantigens
Cytotoxic T-Lymphocytes
Staphylococcus
Natural Killer Cells
Immunoglobulins
Monocytes
Signal Transduction
Blood
B-Lymphocytes
Down-Regulation
Cells
Membranes

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Pulmonary and Respiratory Medicine

Cite this

Human alveolar macrophages inhibit receptor-mediated increases in intracellular calcium concentration in lymphocytes. / Yarbrough, W. C.; Wilkes, D. S.; Weissler, J. C.

In: American Journal of Respiratory Cell and Molecular Biology, Vol. 5, No. 5, 11.1991, p. 411-415.

Research output: Contribution to journalArticle

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