MHC class I is functionally associated with antigen receptors in human T and B lymphomas.

Anders Elm Pedersen; B F Jacoby; S Skov; M H Claesson

doi:10.1006/cimm.1996.0281

MHC class I is functionally associated with antigen receptors in human T and B lymphomas.

Anders Elm Pedersen, B F Jacoby, S Skov, M H Claesson

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

12 Citationer (Scopus)

Abstract

Udgivelsesdato: 1996-Nov-1

Originalsprog	Engelsk
Tidsskrift	Cellular Immunology
Vol/bind	173
Udgave nummer	2
Sider (fra-til)	295-302
Antal sider	7
ISSN	0008-8749
DOI	https://doi.org/10.1006/cimm.1996.0281
Status	Udgivet - 1996

Bibliografisk note

Keywords: Antigens, CD; Antigens, Differentiation, T-Lymphocyte; Calcium; Histocompatibility Antigens Class I; Humans; Jurkat Cells; Lymphocyte Activation; Receptors, Antigen, B-Cell; Receptors, Antigen, T-Cell; Tumor Cells, Cultured; Up-Regulation

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10.1006/cimm.1996.0281

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Citationsformater

@article{5d32bb50ac0611ddb5e9000ea68e967b,

title = "MHC class I is functionally associated with antigen receptors in human T and B lymphomas.",

abstract = "We have studied the antibody-induced effect of cross-linking the major histocompatibility complex class I (MHC-I) in human T leukemic cells (Jurkat) and human B lymphoma cells (Solubo, Burkitts lymphoma) on intracellular [Ca2+]i levels. The increase in [Ca2+]i after MHC-I cross-linking in Jurkat cells and Solubo cells was dependent on both intra- and extracellular Ca2+ stores. The initial increase was dependent on intracellular stores but the long-term elevated [Ca2+]i level was due to an influx of Ca2+. The kinetics of Ca2+ release and influx was different in the two cell lines. In both cell lines the increase in [Ca2+]i after MHC-I cross-linking caused upregulation of CD69, an early marker of activation. When studying the effect of MHC-I cross-linking on the TCR- and B cell antigen receptor (BCR)- mediated increase in [Ca2+]i, respectively, we observed that MHC-I had a costimulatory effect on the TCR-mediated increase in [Ca2+]i in Jurkat cells but not on the anti-IgM-mediated activity of Solubo cells. Studies of subpopulations of Jurkat and Solubo cells expressing different levels of MHC-I on their cell surfaces revealed that the TCR- and BCR-mediated increases in [Ca2+]i, respectively, were positively correlated with the level of MHC-I expressed on the cell surface. These observations suggest two different roles in signal transduction for the MHC-I molecules in the T and B cells studied. First, by themselves MHC-I complexes are able to induce activation of intracellular second messenger systems following cross-linking. Second, threshold levels for activation through antigen receptors in T and B cells are dependent on or determined by the actual numbers of MHC-I complexes present in the cell membrane. Thus the present data strongly point to a new, physiological role for MHC-I molecules in T and B cells.",

author = "Pedersen, {Anders Elm} and Jacoby, {B F} and S Skov and Claesson, {M H}",

note = "Keywords: Antigens, CD; Antigens, Differentiation, T-Lymphocyte; Calcium; Histocompatibility Antigens Class I; Humans; Jurkat Cells; Lymphocyte Activation; Receptors, Antigen, B-Cell; Receptors, Antigen, T-Cell; Tumor Cells, Cultured; Up-Regulation",

year = "1996",

doi = "10.1006/cimm.1996.0281",

language = "English",

volume = "173",

pages = "295--302",

journal = "Cellular Immunology",

issn = "0008-8749",

publisher = "Academic Press",

number = "2",

}

TY - JOUR

T1 - MHC class I is functionally associated with antigen receptors in human T and B lymphomas.

AU - Pedersen, Anders Elm

AU - Jacoby, B F

AU - Skov, S

AU - Claesson, M H

N1 - Keywords: Antigens, CD; Antigens, Differentiation, T-Lymphocyte; Calcium; Histocompatibility Antigens Class I; Humans; Jurkat Cells; Lymphocyte Activation; Receptors, Antigen, B-Cell; Receptors, Antigen, T-Cell; Tumor Cells, Cultured; Up-Regulation

PY - 1996

Y1 - 1996

N2 - We have studied the antibody-induced effect of cross-linking the major histocompatibility complex class I (MHC-I) in human T leukemic cells (Jurkat) and human B lymphoma cells (Solubo, Burkitts lymphoma) on intracellular [Ca2+]i levels. The increase in [Ca2+]i after MHC-I cross-linking in Jurkat cells and Solubo cells was dependent on both intra- and extracellular Ca2+ stores. The initial increase was dependent on intracellular stores but the long-term elevated [Ca2+]i level was due to an influx of Ca2+. The kinetics of Ca2+ release and influx was different in the two cell lines. In both cell lines the increase in [Ca2+]i after MHC-I cross-linking caused upregulation of CD69, an early marker of activation. When studying the effect of MHC-I cross-linking on the TCR- and B cell antigen receptor (BCR)- mediated increase in [Ca2+]i, respectively, we observed that MHC-I had a costimulatory effect on the TCR-mediated increase in [Ca2+]i in Jurkat cells but not on the anti-IgM-mediated activity of Solubo cells. Studies of subpopulations of Jurkat and Solubo cells expressing different levels of MHC-I on their cell surfaces revealed that the TCR- and BCR-mediated increases in [Ca2+]i, respectively, were positively correlated with the level of MHC-I expressed on the cell surface. These observations suggest two different roles in signal transduction for the MHC-I molecules in the T and B cells studied. First, by themselves MHC-I complexes are able to induce activation of intracellular second messenger systems following cross-linking. Second, threshold levels for activation through antigen receptors in T and B cells are dependent on or determined by the actual numbers of MHC-I complexes present in the cell membrane. Thus the present data strongly point to a new, physiological role for MHC-I molecules in T and B cells.

AB - We have studied the antibody-induced effect of cross-linking the major histocompatibility complex class I (MHC-I) in human T leukemic cells (Jurkat) and human B lymphoma cells (Solubo, Burkitts lymphoma) on intracellular [Ca2+]i levels. The increase in [Ca2+]i after MHC-I cross-linking in Jurkat cells and Solubo cells was dependent on both intra- and extracellular Ca2+ stores. The initial increase was dependent on intracellular stores but the long-term elevated [Ca2+]i level was due to an influx of Ca2+. The kinetics of Ca2+ release and influx was different in the two cell lines. In both cell lines the increase in [Ca2+]i after MHC-I cross-linking caused upregulation of CD69, an early marker of activation. When studying the effect of MHC-I cross-linking on the TCR- and B cell antigen receptor (BCR)- mediated increase in [Ca2+]i, respectively, we observed that MHC-I had a costimulatory effect on the TCR-mediated increase in [Ca2+]i in Jurkat cells but not on the anti-IgM-mediated activity of Solubo cells. Studies of subpopulations of Jurkat and Solubo cells expressing different levels of MHC-I on their cell surfaces revealed that the TCR- and BCR-mediated increases in [Ca2+]i, respectively, were positively correlated with the level of MHC-I expressed on the cell surface. These observations suggest two different roles in signal transduction for the MHC-I molecules in the T and B cells studied. First, by themselves MHC-I complexes are able to induce activation of intracellular second messenger systems following cross-linking. Second, threshold levels for activation through antigen receptors in T and B cells are dependent on or determined by the actual numbers of MHC-I complexes present in the cell membrane. Thus the present data strongly point to a new, physiological role for MHC-I molecules in T and B cells.

U2 - 10.1006/cimm.1996.0281

DO - 10.1006/cimm.1996.0281

M3 - Journal article

C2 - 8912890

SN - 0008-8749

VL - 173

SP - 295

EP - 302

JO - Cellular Immunology

JF - Cellular Immunology

IS - 2

ER -