Selective regulation of ICAM‐1 and major histocompatibility complex class I and II molecule expression on epidermal Langerhans cells by some of the cytokines released by keratinocytes and T cells

Chung‐Hsing ‐H Chang, Masutaka Furue, Kunihiko Tamaki

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Abstract

Epidermal Langerhans cells (LC) are major histocompatibility complex (MHC) class II (Ia)‐positive dendritic cells that act as potent antigen‐presenting or accessory cells for primary and secondary T cell‐dependent immune responses. Recent studies have disclosed that the morphological, functional, and phenotypic characteristics of LC are variably and drastically modulated by external stimuli both in vivo and in vitro. However, little is known of the biological significance of diverse cytokines in regulating the surface molecules of LC. To determine the regulatory properties of ICAM‐1, Ia, and MHC class I (H‐2K) molecules in LC, we have examined the effects of interleukin (IL)‐1α, IL‐1β, IL‐2, IL‐3, IL‐4, IL‐5, IL‐6, IL‐7, IL‐10, interferon‐γ (IFN‐γ), tumor necrosis factor‐α (TNF‐α), and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) on the expression of these molecules. Among the cytokines examined, IFN‐γ markedly and reproducibly up‐regulates the expression of H‐2K, but not ICAM‐1, in Ia + LC in a time‐ and dose‐dependent manner. TNF‐α consistently up‐regulates the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 slightly but reproducibly inhibits the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 potently inhibits the TNF‐α‐induced ICAM‐1 up‐regulation, but not the IFN‐γ‐induced H‐2K up‐regulation. Moreover, no cytokine consistently affects the Ia expression of LC. In addition, slight enhancing effects have been observed on H‐2K expression by IL‐4, and on ICAM‐1 expression by IL‐1α, IL‐1β, or GM‐CSF. The present data suggest that the selective regulation is operative in a certain cell surface moiety of LC by various cytokines. These results further facilitate our understanding of immunobiology of LC.

Original languageEnglish
Pages (from-to)2889-2895
Number of pages7
JournalEuropean Journal of Immunology
Volume24
Issue number11
DOIs
Publication statusPublished - Jan 1 1994
Externally publishedYes

Fingerprint

Langerhans Cells
Major Histocompatibility Complex
Keratinocytes
Cytokines
T-Lymphocytes
Up-Regulation
Interleukin-10
Interleukin-4
Interferons
Tumor Necrosis Factor-alpha
Interleukin-7
Interleukin-5
Interleukin-1
Dendritic Cells
Interleukin-2
Interleukin-6

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

@article{3dfa27a8f56f4cc89a7b8eacf692bea6,
title = "Selective regulation of ICAM‐1 and major histocompatibility complex class I and II molecule expression on epidermal Langerhans cells by some of the cytokines released by keratinocytes and T cells",
abstract = "Epidermal Langerhans cells (LC) are major histocompatibility complex (MHC) class II (Ia)‐positive dendritic cells that act as potent antigen‐presenting or accessory cells for primary and secondary T cell‐dependent immune responses. Recent studies have disclosed that the morphological, functional, and phenotypic characteristics of LC are variably and drastically modulated by external stimuli both in vivo and in vitro. However, little is known of the biological significance of diverse cytokines in regulating the surface molecules of LC. To determine the regulatory properties of ICAM‐1, Ia, and MHC class I (H‐2K) molecules in LC, we have examined the effects of interleukin (IL)‐1α, IL‐1β, IL‐2, IL‐3, IL‐4, IL‐5, IL‐6, IL‐7, IL‐10, interferon‐γ (IFN‐γ), tumor necrosis factor‐α (TNF‐α), and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) on the expression of these molecules. Among the cytokines examined, IFN‐γ markedly and reproducibly up‐regulates the expression of H‐2K, but not ICAM‐1, in Ia + LC in a time‐ and dose‐dependent manner. TNF‐α consistently up‐regulates the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 slightly but reproducibly inhibits the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 potently inhibits the TNF‐α‐induced ICAM‐1 up‐regulation, but not the IFN‐γ‐induced H‐2K up‐regulation. Moreover, no cytokine consistently affects the Ia expression of LC. In addition, slight enhancing effects have been observed on H‐2K expression by IL‐4, and on ICAM‐1 expression by IL‐1α, IL‐1β, or GM‐CSF. The present data suggest that the selective regulation is operative in a certain cell surface moiety of LC by various cytokines. These results further facilitate our understanding of immunobiology of LC.",
author = "Chang, {Chung‐Hsing ‐H} and Masutaka Furue and Kunihiko Tamaki",
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T1 - Selective regulation of ICAM‐1 and major histocompatibility complex class I and II molecule expression on epidermal Langerhans cells by some of the cytokines released by keratinocytes and T cells

AU - Chang, Chung‐Hsing ‐H

AU - Furue, Masutaka

AU - Tamaki, Kunihiko

PY - 1994/1/1

Y1 - 1994/1/1

N2 - Epidermal Langerhans cells (LC) are major histocompatibility complex (MHC) class II (Ia)‐positive dendritic cells that act as potent antigen‐presenting or accessory cells for primary and secondary T cell‐dependent immune responses. Recent studies have disclosed that the morphological, functional, and phenotypic characteristics of LC are variably and drastically modulated by external stimuli both in vivo and in vitro. However, little is known of the biological significance of diverse cytokines in regulating the surface molecules of LC. To determine the regulatory properties of ICAM‐1, Ia, and MHC class I (H‐2K) molecules in LC, we have examined the effects of interleukin (IL)‐1α, IL‐1β, IL‐2, IL‐3, IL‐4, IL‐5, IL‐6, IL‐7, IL‐10, interferon‐γ (IFN‐γ), tumor necrosis factor‐α (TNF‐α), and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) on the expression of these molecules. Among the cytokines examined, IFN‐γ markedly and reproducibly up‐regulates the expression of H‐2K, but not ICAM‐1, in Ia + LC in a time‐ and dose‐dependent manner. TNF‐α consistently up‐regulates the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 slightly but reproducibly inhibits the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 potently inhibits the TNF‐α‐induced ICAM‐1 up‐regulation, but not the IFN‐γ‐induced H‐2K up‐regulation. Moreover, no cytokine consistently affects the Ia expression of LC. In addition, slight enhancing effects have been observed on H‐2K expression by IL‐4, and on ICAM‐1 expression by IL‐1α, IL‐1β, or GM‐CSF. The present data suggest that the selective regulation is operative in a certain cell surface moiety of LC by various cytokines. These results further facilitate our understanding of immunobiology of LC.

AB - Epidermal Langerhans cells (LC) are major histocompatibility complex (MHC) class II (Ia)‐positive dendritic cells that act as potent antigen‐presenting or accessory cells for primary and secondary T cell‐dependent immune responses. Recent studies have disclosed that the morphological, functional, and phenotypic characteristics of LC are variably and drastically modulated by external stimuli both in vivo and in vitro. However, little is known of the biological significance of diverse cytokines in regulating the surface molecules of LC. To determine the regulatory properties of ICAM‐1, Ia, and MHC class I (H‐2K) molecules in LC, we have examined the effects of interleukin (IL)‐1α, IL‐1β, IL‐2, IL‐3, IL‐4, IL‐5, IL‐6, IL‐7, IL‐10, interferon‐γ (IFN‐γ), tumor necrosis factor‐α (TNF‐α), and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) on the expression of these molecules. Among the cytokines examined, IFN‐γ markedly and reproducibly up‐regulates the expression of H‐2K, but not ICAM‐1, in Ia + LC in a time‐ and dose‐dependent manner. TNF‐α consistently up‐regulates the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 slightly but reproducibly inhibits the expression of ICAM‐1, but not H‐2K, in a time‐ and dose‐dependent manner. IL‐10 potently inhibits the TNF‐α‐induced ICAM‐1 up‐regulation, but not the IFN‐γ‐induced H‐2K up‐regulation. Moreover, no cytokine consistently affects the Ia expression of LC. In addition, slight enhancing effects have been observed on H‐2K expression by IL‐4, and on ICAM‐1 expression by IL‐1α, IL‐1β, or GM‐CSF. The present data suggest that the selective regulation is operative in a certain cell surface moiety of LC by various cytokines. These results further facilitate our understanding of immunobiology of LC.

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