Human recombinant interferon-β influences T helper subset differentiation by regulating cytokine secretion pattern and expression of homing receptors

Bradford L. McRae, Louis Picker, Gijs A. Van Seventer

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Type I interferons (IFN) are important regulators of both innate and acquired immunity. We have used an in vitro system of human CD4+. T cell differentiation to determine how IFN-β influences development of T helper (Th) subsets and homing receptor expression. IFN-β promoted differentiation of CD4+. T cells that produce low levels of both IFN-γ and lymphotoxin compared to interleukin (IL)-12-derived Th1 CD4+ T cells. IFN-β inhibited production of Th2 cytokines (IL-5 and IL-13) and augmented IL-12-mediated IL-10 secretion. In addition. IFN-β significantly enhanced L-selectin expression on CD4+ T cells and synergized with IL-12 to induce expression of cutaneous lymphocyte-associated antigen (CLA). This Th1 L-selectin+, CLA+ phenotype is characteristic of T cells found in normal human skin and suggests a role for type T IFN in the regulation of Th subset differentiation and tissue-specific homing receptors.

Original languageEnglish (US)
Pages (from-to)2650-2656
Number of pages7
JournalEuropean Journal of Immunology
Volume27
Issue number10
DOIs
StatePublished - Oct 1997
Externally publishedYes

Fingerprint

Interferons
Cytokines
T-Lymphocytes
Interleukin-12
L-Selectin
Skin
Lymphocytes
Antigens
Lymphotoxin-alpha
Interferon Type I
Interleukin-13
Interleukin-5
Adaptive Immunity
Innate Immunity
Interleukin-10
Cell Differentiation
Phenotype

Keywords

  • Cytokine
  • Homing
  • Human
  • Interferon-β
  • T lymphocyte

ASJC Scopus subject areas

  • Immunology

Cite this

Human recombinant interferon-β influences T helper subset differentiation by regulating cytokine secretion pattern and expression of homing receptors. / McRae, Bradford L.; Picker, Louis; Van Seventer, Gijs A.

In: European Journal of Immunology, Vol. 27, No. 10, 10.1997, p. 2650-2656.

Research output: Contribution to journalArticle

@article{0ca855ccd25c4f6eb10200ceead24d14,
title = "Human recombinant interferon-β influences T helper subset differentiation by regulating cytokine secretion pattern and expression of homing receptors",
abstract = "Type I interferons (IFN) are important regulators of both innate and acquired immunity. We have used an in vitro system of human CD4+. T cell differentiation to determine how IFN-β influences development of T helper (Th) subsets and homing receptor expression. IFN-β promoted differentiation of CD4+. T cells that produce low levels of both IFN-γ and lymphotoxin compared to interleukin (IL)-12-derived Th1 CD4+ T cells. IFN-β inhibited production of Th2 cytokines (IL-5 and IL-13) and augmented IL-12-mediated IL-10 secretion. In addition. IFN-β significantly enhanced L-selectin expression on CD4+ T cells and synergized with IL-12 to induce expression of cutaneous lymphocyte-associated antigen (CLA). This Th1 L-selectin+, CLA+ phenotype is characteristic of T cells found in normal human skin and suggests a role for type T IFN in the regulation of Th subset differentiation and tissue-specific homing receptors.",
keywords = "Cytokine, Homing, Human, Interferon-β, T lymphocyte",
author = "McRae, {Bradford L.} and Louis Picker and {Van Seventer}, {Gijs A.}",
year = "1997",
month = "10",
doi = "10.1002/eji.1830271026",
language = "English (US)",
volume = "27",
pages = "2650--2656",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag",
number = "10",

}

TY - JOUR

T1 - Human recombinant interferon-β influences T helper subset differentiation by regulating cytokine secretion pattern and expression of homing receptors

AU - McRae, Bradford L.

AU - Picker, Louis

AU - Van Seventer, Gijs A.

PY - 1997/10

Y1 - 1997/10

N2 - Type I interferons (IFN) are important regulators of both innate and acquired immunity. We have used an in vitro system of human CD4+. T cell differentiation to determine how IFN-β influences development of T helper (Th) subsets and homing receptor expression. IFN-β promoted differentiation of CD4+. T cells that produce low levels of both IFN-γ and lymphotoxin compared to interleukin (IL)-12-derived Th1 CD4+ T cells. IFN-β inhibited production of Th2 cytokines (IL-5 and IL-13) and augmented IL-12-mediated IL-10 secretion. In addition. IFN-β significantly enhanced L-selectin expression on CD4+ T cells and synergized with IL-12 to induce expression of cutaneous lymphocyte-associated antigen (CLA). This Th1 L-selectin+, CLA+ phenotype is characteristic of T cells found in normal human skin and suggests a role for type T IFN in the regulation of Th subset differentiation and tissue-specific homing receptors.

AB - Type I interferons (IFN) are important regulators of both innate and acquired immunity. We have used an in vitro system of human CD4+. T cell differentiation to determine how IFN-β influences development of T helper (Th) subsets and homing receptor expression. IFN-β promoted differentiation of CD4+. T cells that produce low levels of both IFN-γ and lymphotoxin compared to interleukin (IL)-12-derived Th1 CD4+ T cells. IFN-β inhibited production of Th2 cytokines (IL-5 and IL-13) and augmented IL-12-mediated IL-10 secretion. In addition. IFN-β significantly enhanced L-selectin expression on CD4+ T cells and synergized with IL-12 to induce expression of cutaneous lymphocyte-associated antigen (CLA). This Th1 L-selectin+, CLA+ phenotype is characteristic of T cells found in normal human skin and suggests a role for type T IFN in the regulation of Th subset differentiation and tissue-specific homing receptors.

KW - Cytokine

KW - Homing

KW - Human

KW - Interferon-β

KW - T lymphocyte

UR - http://www.scopus.com/inward/record.url?scp=0030658048&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030658048&partnerID=8YFLogxK

U2 - 10.1002/eji.1830271026

DO - 10.1002/eji.1830271026

M3 - Article

VL - 27

SP - 2650

EP - 2656

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 10

ER -