TY - JOUR
T1 - Human alveolar macrophages inhibit receptor-mediated increases in intracellular calcium concentration in lymphocytes.
AU - Yarbrough, W. C.
AU - Wilkes, D. S.
AU - Weissler, J. C.
PY - 1991/11
Y1 - 1991/11
N2 - 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.
AB - 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.
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U2 - 10.1165/ajrcmb/5.5.411
DO - 10.1165/ajrcmb/5.5.411
M3 - Article
C2 - 1657060
AN - SCOPUS:0026261689
SN - 1044-1549
VL - 5
SP - 411
EP - 415
JO - American journal of respiratory cell and molecular biology
JF - American journal of respiratory cell and molecular biology
IS - 5
ER -