Macrophage inflammatory protein-1α rapidly modulates its receptors and inhibits the anti-CD3 mAb-mediated proliferation of T lymphocytes

Z. Zhou, Y. J. Kim, Karen Pollok, J. Hurtado, J. K. Lee, Hal Broxmeyer, B. S. Kwon

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Macrophage inflammatory protein-1α (MIP-1α) is a member of the intercrine/chemokine family which consists of basic, heparin-binding, small molecular weight proteins. We have previously shown that a T cell line, CTLL- R8, carried high-affinity receptors for MIP-1α and the proliferation of CTLL-R8 cells was inhibited by murine recombinant (mr) MIP-1α. We extended our previous studies to murine resting splenic T lymphocytes to determine whether the inhibition of T cell proliferation is a general property of MIP- 1α. The resting splenic T cells carried approximately 680 high-affinity binding sites for mrMIP-1α; more than 90% of the primary T cells carried MIP-1α receptors. When the T cells were stimulated with immobilized anti- CD3 mAb in the presence of accessory cells, the MIP-1α binding was reduced. The lowest binding was obtained 2 h after anti-CD3 mAb stimulation due to the internalization of MIP-1α receptors. mrMIP-1α inhibited the anti-CD3 mAb- mediated proliferation of murine splenic T lymphocytes. The maximum inhibition was obtained when mrMIP-1α was added 30 min before anti-CD3 mAb stimulation. Slight inhibition of T cell proliferation was observed when mrMIP-1α was added at the same time as anti-CD3 mAb stimulation. These results indicate that T lymphocytes are regulated negatively by MIP-1α, which occurs when the T cells are exposed to MIP-1α before activation. The negative effect of MIP-1α seems to be mediated in part by the inhibition of IL-2 production, for there was a reduction in both the IL-2 mRNA levels and the IL-2 activity in supernatants from T cells preincubated with MIP-1α before anti-CD3 mAb stimulation.

Original languageEnglish
Pages (from-to)4333-4341
Number of pages9
JournalJournal of Immunology
Volume151
Issue number8
StatePublished - 1993

Fingerprint

Macrophage Inflammatory Proteins
T-Lymphocytes
Interleukin-2
Chemokines
Cell Proliferation
Recombinant Proteins
Protein Binding
Heparin
Molecular Weight
Binding Sites

ASJC Scopus subject areas

  • Immunology

Cite this

Macrophage inflammatory protein-1α rapidly modulates its receptors and inhibits the anti-CD3 mAb-mediated proliferation of T lymphocytes. / Zhou, Z.; Kim, Y. J.; Pollok, Karen; Hurtado, J.; Lee, J. K.; Broxmeyer, Hal; Kwon, B. S.

In: Journal of Immunology, Vol. 151, No. 8, 1993, p. 4333-4341.

Research output: Contribution to journalArticle

@article{77a6adba27424879aae9ba878cd298ba,
title = "Macrophage inflammatory protein-1α rapidly modulates its receptors and inhibits the anti-CD3 mAb-mediated proliferation of T lymphocytes",
abstract = "Macrophage inflammatory protein-1α (MIP-1α) is a member of the intercrine/chemokine family which consists of basic, heparin-binding, small molecular weight proteins. We have previously shown that a T cell line, CTLL- R8, carried high-affinity receptors for MIP-1α and the proliferation of CTLL-R8 cells was inhibited by murine recombinant (mr) MIP-1α. We extended our previous studies to murine resting splenic T lymphocytes to determine whether the inhibition of T cell proliferation is a general property of MIP- 1α. The resting splenic T cells carried approximately 680 high-affinity binding sites for mrMIP-1α; more than 90{\%} of the primary T cells carried MIP-1α receptors. When the T cells were stimulated with immobilized anti- CD3 mAb in the presence of accessory cells, the MIP-1α binding was reduced. The lowest binding was obtained 2 h after anti-CD3 mAb stimulation due to the internalization of MIP-1α receptors. mrMIP-1α inhibited the anti-CD3 mAb- mediated proliferation of murine splenic T lymphocytes. The maximum inhibition was obtained when mrMIP-1α was added 30 min before anti-CD3 mAb stimulation. Slight inhibition of T cell proliferation was observed when mrMIP-1α was added at the same time as anti-CD3 mAb stimulation. These results indicate that T lymphocytes are regulated negatively by MIP-1α, which occurs when the T cells are exposed to MIP-1α before activation. The negative effect of MIP-1α seems to be mediated in part by the inhibition of IL-2 production, for there was a reduction in both the IL-2 mRNA levels and the IL-2 activity in supernatants from T cells preincubated with MIP-1α before anti-CD3 mAb stimulation.",
author = "Z. Zhou and Kim, {Y. J.} and Karen Pollok and J. Hurtado and Lee, {J. K.} and Hal Broxmeyer and Kwon, {B. S.}",
year = "1993",
language = "English",
volume = "151",
pages = "4333--4341",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "8",

}

TY - JOUR

T1 - Macrophage inflammatory protein-1α rapidly modulates its receptors and inhibits the anti-CD3 mAb-mediated proliferation of T lymphocytes

AU - Zhou, Z.

AU - Kim, Y. J.

AU - Pollok, Karen

AU - Hurtado, J.

AU - Lee, J. K.

AU - Broxmeyer, Hal

AU - Kwon, B. S.

PY - 1993

Y1 - 1993

N2 - Macrophage inflammatory protein-1α (MIP-1α) is a member of the intercrine/chemokine family which consists of basic, heparin-binding, small molecular weight proteins. We have previously shown that a T cell line, CTLL- R8, carried high-affinity receptors for MIP-1α and the proliferation of CTLL-R8 cells was inhibited by murine recombinant (mr) MIP-1α. We extended our previous studies to murine resting splenic T lymphocytes to determine whether the inhibition of T cell proliferation is a general property of MIP- 1α. The resting splenic T cells carried approximately 680 high-affinity binding sites for mrMIP-1α; more than 90% of the primary T cells carried MIP-1α receptors. When the T cells were stimulated with immobilized anti- CD3 mAb in the presence of accessory cells, the MIP-1α binding was reduced. The lowest binding was obtained 2 h after anti-CD3 mAb stimulation due to the internalization of MIP-1α receptors. mrMIP-1α inhibited the anti-CD3 mAb- mediated proliferation of murine splenic T lymphocytes. The maximum inhibition was obtained when mrMIP-1α was added 30 min before anti-CD3 mAb stimulation. Slight inhibition of T cell proliferation was observed when mrMIP-1α was added at the same time as anti-CD3 mAb stimulation. These results indicate that T lymphocytes are regulated negatively by MIP-1α, which occurs when the T cells are exposed to MIP-1α before activation. The negative effect of MIP-1α seems to be mediated in part by the inhibition of IL-2 production, for there was a reduction in both the IL-2 mRNA levels and the IL-2 activity in supernatants from T cells preincubated with MIP-1α before anti-CD3 mAb stimulation.

AB - Macrophage inflammatory protein-1α (MIP-1α) is a member of the intercrine/chemokine family which consists of basic, heparin-binding, small molecular weight proteins. We have previously shown that a T cell line, CTLL- R8, carried high-affinity receptors for MIP-1α and the proliferation of CTLL-R8 cells was inhibited by murine recombinant (mr) MIP-1α. We extended our previous studies to murine resting splenic T lymphocytes to determine whether the inhibition of T cell proliferation is a general property of MIP- 1α. The resting splenic T cells carried approximately 680 high-affinity binding sites for mrMIP-1α; more than 90% of the primary T cells carried MIP-1α receptors. When the T cells were stimulated with immobilized anti- CD3 mAb in the presence of accessory cells, the MIP-1α binding was reduced. The lowest binding was obtained 2 h after anti-CD3 mAb stimulation due to the internalization of MIP-1α receptors. mrMIP-1α inhibited the anti-CD3 mAb- mediated proliferation of murine splenic T lymphocytes. The maximum inhibition was obtained when mrMIP-1α was added 30 min before anti-CD3 mAb stimulation. Slight inhibition of T cell proliferation was observed when mrMIP-1α was added at the same time as anti-CD3 mAb stimulation. These results indicate that T lymphocytes are regulated negatively by MIP-1α, which occurs when the T cells are exposed to MIP-1α before activation. The negative effect of MIP-1α seems to be mediated in part by the inhibition of IL-2 production, for there was a reduction in both the IL-2 mRNA levels and the IL-2 activity in supernatants from T cells preincubated with MIP-1α before anti-CD3 mAb stimulation.

UR - http://www.scopus.com/inward/record.url?scp=0027521301&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027521301&partnerID=8YFLogxK

M3 - Article

C2 - 8409405

AN - SCOPUS:0027521301

VL - 151

SP - 4333

EP - 4341

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 8

ER -