Inhibition of lymphokine-activated killer cells by human pulmonary macrophages

discordance between up-regulation of the beta chain (p75) of the interleukin-2 receptor on CD56+ cells and limited response to interleukin-2.

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

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Previous studies have demonstrated that interaction of interleukin-2 (IL-2) with the beta chain (p75) of the IL-2 receptor on CD56+ cells is necessary for the development of lymphokine-activated killer (LAK) activity and proliferation of CD56+ LAK cells in response to IL-2. Human pulmonary macrophages (PM) are potent inhibitors of LAK cells in vitro, and purified resident human lung lymphocytes show limited LAK activity in response to IL-2, suggesting that IL-2-p75 interactions may be altered locally in vivo. In the current study, human PM or anti-p75 inhibited LAK activity and proliferation of CD56+ cells in response to IL-2. This effect was produced by either live or paraformaldehyde-fixed PM, but not peripheral blood monocytes, suggesting that a membrane signal on PM was responsible for inhibition. Suppression of LAK function and proliferation in response to IL-2 occurred despite a rapid up-regulation of p75 on CD56+ cells after 24 h of incubation with PM. Greater than 70% of CD56+ cells expressed p75 after culture with either live or fixed PM, compared with 10 to 15% at 0 h or after 24 h of incubation in IL-2 alone. p75 dim and p75 bright cells increased equally, suggesting that p75 was being up-regulated on previously p75- cells rather than an overexpansion of one subset of p75+ cells. The increase in p75 expression in the presence of PM paralleled with an increase in IL-2 binding to these lymphocytes. These results suggest that PM inhibit the activation of LAK cells at a point distal to IL-2-p75 binding.

Original languageEnglish (US)
Pages (from-to)184-191
Number of pages8
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume10
Issue number2
StatePublished - Feb 1994
Externally publishedYes

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Interleukin-2 Receptor beta Subunit
Lymphokine-Activated Killer Cells
Lymphokines
Interleukin-2 Receptors
Alveolar Macrophages
Interleukin-2
Up-Regulation
Lymphocytes
Macrophage Activation
Monocytes
Blood
Chemical activation
Cell Proliferation

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Pulmonary and Respiratory Medicine

Cite this

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title = "Inhibition of lymphokine-activated killer cells by human pulmonary macrophages: discordance between up-regulation of the beta chain (p75) of the interleukin-2 receptor on CD56+ cells and limited response to interleukin-2.",
abstract = "Previous studies have demonstrated that interaction of interleukin-2 (IL-2) with the beta chain (p75) of the IL-2 receptor on CD56+ cells is necessary for the development of lymphokine-activated killer (LAK) activity and proliferation of CD56+ LAK cells in response to IL-2. Human pulmonary macrophages (PM) are potent inhibitors of LAK cells in vitro, and purified resident human lung lymphocytes show limited LAK activity in response to IL-2, suggesting that IL-2-p75 interactions may be altered locally in vivo. In the current study, human PM or anti-p75 inhibited LAK activity and proliferation of CD56+ cells in response to IL-2. This effect was produced by either live or paraformaldehyde-fixed PM, but not peripheral blood monocytes, suggesting that a membrane signal on PM was responsible for inhibition. Suppression of LAK function and proliferation in response to IL-2 occurred despite a rapid up-regulation of p75 on CD56+ cells after 24 h of incubation with PM. Greater than 70{\%} of CD56+ cells expressed p75 after culture with either live or fixed PM, compared with 10 to 15{\%} at 0 h or after 24 h of incubation in IL-2 alone. p75 dim and p75 bright cells increased equally, suggesting that p75 was being up-regulated on previously p75- cells rather than an overexpansion of one subset of p75+ cells. The increase in p75 expression in the presence of PM paralleled with an increase in IL-2 binding to these lymphocytes. These results suggest that PM inhibit the activation of LAK cells at a point distal to IL-2-p75 binding.",
author = "Yarbrough, {W. C.} and Wilkes, {D. S.} and Weissler, {J. C.}",
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T2 - discordance between up-regulation of the beta chain (p75) of the interleukin-2 receptor on CD56+ cells and limited response to interleukin-2.

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AU - Wilkes, D. S.

AU - Weissler, J. C.

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N2 - Previous studies have demonstrated that interaction of interleukin-2 (IL-2) with the beta chain (p75) of the IL-2 receptor on CD56+ cells is necessary for the development of lymphokine-activated killer (LAK) activity and proliferation of CD56+ LAK cells in response to IL-2. Human pulmonary macrophages (PM) are potent inhibitors of LAK cells in vitro, and purified resident human lung lymphocytes show limited LAK activity in response to IL-2, suggesting that IL-2-p75 interactions may be altered locally in vivo. In the current study, human PM or anti-p75 inhibited LAK activity and proliferation of CD56+ cells in response to IL-2. This effect was produced by either live or paraformaldehyde-fixed PM, but not peripheral blood monocytes, suggesting that a membrane signal on PM was responsible for inhibition. Suppression of LAK function and proliferation in response to IL-2 occurred despite a rapid up-regulation of p75 on CD56+ cells after 24 h of incubation with PM. Greater than 70% of CD56+ cells expressed p75 after culture with either live or fixed PM, compared with 10 to 15% at 0 h or after 24 h of incubation in IL-2 alone. p75 dim and p75 bright cells increased equally, suggesting that p75 was being up-regulated on previously p75- cells rather than an overexpansion of one subset of p75+ cells. The increase in p75 expression in the presence of PM paralleled with an increase in IL-2 binding to these lymphocytes. These results suggest that PM inhibit the activation of LAK cells at a point distal to IL-2-p75 binding.

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