Negative regulation of rat natural killer cell activity by major histocompatibility complex class I recognition

Elmar Kraus, Doris Lambracht, Kurt Wonigeit, Thomas Hünig

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

The cytolytic activity of human and mouse natural killer (NK) cells is negatively regulated by self major histocompatibility complex (MHC) class I molecules on potential target cells. In the rat, protection by RT1 class I gene products has so far not been formally shown although the complex effects of foreign and self RT1 genes on polyclonal NK cell activity suggest that MHC recognition can have both stimulatory and inhibitory effects. Here we report that the expression of self-MHC class I molecules on target cells strongly inhibits lysis by a long term NK cell line derived from LEW (RT1(l)) rats and by LEW NK cells activated by short-term culture in the presence of interleukin-2. This was demonstrated with mouse-rat hybridoma target cells expressing different rat MHC alleles and with mouse tumor target cells transfected with classical (RT1.A(l)) and nonclassical (RT1.C(l)) rat MHC class I genes. With hybridoma target cells, the strongest reduction in lysis as compared to the parental mouse myeloma line was observed when 'self' (LEW) MHC was expressed, while hybridomas expressing other MHC alleles showed less and variable reduction. Transfection of RT1.A(l) protected both L-929 fibroblasts and P815 mastocytoma cells from lysis by the NK cell line, while RT1. C(l) only protected P815 cells, indicating that additional target cell properties regulate rat NK cell activity.

Original languageEnglish (US)
Pages (from-to)2582-2586
Number of pages5
JournalEuropean Journal of Immunology
Volume26
Issue number11
DOIs
StatePublished - 1996

Fingerprint

Major Histocompatibility Complex
Natural Killer Cells
Hybridomas
MHC Class I Genes
Alleles
Mastocytoma
Cell Line
Human Activities
Self Report
Interleukin-2
Transfection
Fibroblasts
Genes
Neoplasms

Keywords

  • Major histocompatibility complex
  • Natural killer cell
  • Rat

ASJC Scopus subject areas

  • Immunology

Cite this

Negative regulation of rat natural killer cell activity by major histocompatibility complex class I recognition. / Kraus, Elmar; Lambracht, Doris; Wonigeit, Kurt; Hünig, Thomas.

In: European Journal of Immunology, Vol. 26, No. 11, 1996, p. 2582-2586.

Research output: Contribution to journalArticle

@article{7238c65113974afca16fffb483133ad6,
title = "Negative regulation of rat natural killer cell activity by major histocompatibility complex class I recognition",
abstract = "The cytolytic activity of human and mouse natural killer (NK) cells is negatively regulated by self major histocompatibility complex (MHC) class I molecules on potential target cells. In the rat, protection by RT1 class I gene products has so far not been formally shown although the complex effects of foreign and self RT1 genes on polyclonal NK cell activity suggest that MHC recognition can have both stimulatory and inhibitory effects. Here we report that the expression of self-MHC class I molecules on target cells strongly inhibits lysis by a long term NK cell line derived from LEW (RT1(l)) rats and by LEW NK cells activated by short-term culture in the presence of interleukin-2. This was demonstrated with mouse-rat hybridoma target cells expressing different rat MHC alleles and with mouse tumor target cells transfected with classical (RT1.A(l)) and nonclassical (RT1.C(l)) rat MHC class I genes. With hybridoma target cells, the strongest reduction in lysis as compared to the parental mouse myeloma line was observed when 'self' (LEW) MHC was expressed, while hybridomas expressing other MHC alleles showed less and variable reduction. Transfection of RT1.A(l) protected both L-929 fibroblasts and P815 mastocytoma cells from lysis by the NK cell line, while RT1. C(l) only protected P815 cells, indicating that additional target cell properties regulate rat NK cell activity.",
keywords = "Major histocompatibility complex, Natural killer cell, Rat",
author = "Elmar Kraus and Doris Lambracht and Kurt Wonigeit and Thomas H{\"u}nig",
year = "1996",
doi = "10.1002/eji.1830261107",
language = "English (US)",
volume = "26",
pages = "2582--2586",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag",
number = "11",

}

TY - JOUR

T1 - Negative regulation of rat natural killer cell activity by major histocompatibility complex class I recognition

AU - Kraus, Elmar

AU - Lambracht, Doris

AU - Wonigeit, Kurt

AU - Hünig, Thomas

PY - 1996

Y1 - 1996

N2 - The cytolytic activity of human and mouse natural killer (NK) cells is negatively regulated by self major histocompatibility complex (MHC) class I molecules on potential target cells. In the rat, protection by RT1 class I gene products has so far not been formally shown although the complex effects of foreign and self RT1 genes on polyclonal NK cell activity suggest that MHC recognition can have both stimulatory and inhibitory effects. Here we report that the expression of self-MHC class I molecules on target cells strongly inhibits lysis by a long term NK cell line derived from LEW (RT1(l)) rats and by LEW NK cells activated by short-term culture in the presence of interleukin-2. This was demonstrated with mouse-rat hybridoma target cells expressing different rat MHC alleles and with mouse tumor target cells transfected with classical (RT1.A(l)) and nonclassical (RT1.C(l)) rat MHC class I genes. With hybridoma target cells, the strongest reduction in lysis as compared to the parental mouse myeloma line was observed when 'self' (LEW) MHC was expressed, while hybridomas expressing other MHC alleles showed less and variable reduction. Transfection of RT1.A(l) protected both L-929 fibroblasts and P815 mastocytoma cells from lysis by the NK cell line, while RT1. C(l) only protected P815 cells, indicating that additional target cell properties regulate rat NK cell activity.

AB - The cytolytic activity of human and mouse natural killer (NK) cells is negatively regulated by self major histocompatibility complex (MHC) class I molecules on potential target cells. In the rat, protection by RT1 class I gene products has so far not been formally shown although the complex effects of foreign and self RT1 genes on polyclonal NK cell activity suggest that MHC recognition can have both stimulatory and inhibitory effects. Here we report that the expression of self-MHC class I molecules on target cells strongly inhibits lysis by a long term NK cell line derived from LEW (RT1(l)) rats and by LEW NK cells activated by short-term culture in the presence of interleukin-2. This was demonstrated with mouse-rat hybridoma target cells expressing different rat MHC alleles and with mouse tumor target cells transfected with classical (RT1.A(l)) and nonclassical (RT1.C(l)) rat MHC class I genes. With hybridoma target cells, the strongest reduction in lysis as compared to the parental mouse myeloma line was observed when 'self' (LEW) MHC was expressed, while hybridomas expressing other MHC alleles showed less and variable reduction. Transfection of RT1.A(l) protected both L-929 fibroblasts and P815 mastocytoma cells from lysis by the NK cell line, while RT1. C(l) only protected P815 cells, indicating that additional target cell properties regulate rat NK cell activity.

KW - Major histocompatibility complex

KW - Natural killer cell

KW - Rat

UR - http://www.scopus.com/inward/record.url?scp=0029908792&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029908792&partnerID=8YFLogxK

U2 - 10.1002/eji.1830261107

DO - 10.1002/eji.1830261107

M3 - Article

C2 - 8921942

AN - SCOPUS:0029908792

VL - 26

SP - 2582

EP - 2586

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 11

ER -