HIGHLY LYTIC CD8+, ALPHA,BETA T-CELL RECEPTOR CYTOTOXIC T-CELLS WITH MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) CLASS-I ANTIGEN-DIRECTED CYTOTOXICITY IN BETA(2)-MICROGLOBULIN, MHC CLASS-I-DEFICIENT MICE

被引：77

作者：

APASOV, S ^{[1
]}

SITKOVSKY, M ^{[1
]}

机构：

[1] NIAID,IMMUNOL LAB,BETHESDA,MD 20892

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 07期

关键词：

GENE KNOCKOUT;

D O I：

10.1073/pnas.90.7.2837

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Targeted disruption of the beta2-microglobulin (beta2m) gene results in major histocompatibility complex (MHC) class I deficiency and virtual disappearance of functional CD8+ cytotoxic T lymphocytes (CTLs) in beta2m-deficient (beta2m -/-) mice. We asked whether the beta2m -/- mice are able to reject tumor cells injected i.p. and what is the cellular composition of peritoneal exudate leukocytes (PELs) from such mice. We found that beta2m -/- mice do reject MHC class I-bearing tumor cells injected i.p. Surprisingly, analysis of PEL CTLs obtained from i.p. tumor-injected beta2m -/- mice revealed the presence of a large proportion of functional, tumor-destroying CD8+, CD4-, alphabeta T-cell receptor-positive, CD3+, Thy-1+, MHC class I-negative CTLs with strong MHC class I-directed cytotoxic activity. These results call for careful studies of local accumulation of CD8+ CTLs in beta2m -/- mouse models and suggest that the dramatic decrease in MHC class I expression caused by beta2m gene disruption does not prevent CD8+/CD4-cell selection and expansion.

引用

页码：2837 / 2841

页数：5

共 21 条

[1] BETA-2-MICROGLOBULIN IS NOT REQUIRED FOR CELL-SURFACE EXPRESSION OF THE MURINE CLASS-I HISTOCOMPATIBILITY ANTIGEN H-2DB OR OF A TRUNCATED H-2DB [J].