Regulation of class II MHC expression

被引:55
作者
Rohn, WM
Lee, YJ
Benveniste, EN
机构
[1] UNIV ALABAMA, DEPT PHYSIOL & BIOPHYS, BIRMINGHAM, AL 35294 USA
[2] UNIV ALABAMA, DEPT CELL BIOL, BIRMINGHAM, AL 35294 USA
关键词
antigen presentation; cytokines; CIITA; autoimmunity; signal transduction; transcription factors;
D O I
10.1615/CritRevImmunol.v16.i3.40
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The class II genes of the major histocompatibility complex (MIC) encode the alpha/beta heterodimeric glycoproteins that play a critical role in the induction of immune responses through presentation of processed antigen to CD4+ T lymphocytes. The constitutive expression of class II MHC antigens is restricted primarily to B cells, dendritic cells, thymic epithelium, and macrophages, although a wide variety of other cell types can be induced to express class II antigens after exposure to cytokines. The appropriate constitutive and inducible expression of class II MHC antigens is essential for normal immune function; thus, it is not surprising that aberrant expression on cell types normally class II MHC negative has been correlated with various autoimmune disorders, and lack of expression results in a severe combined immunodeficiency disorder called bare lymphocyte syndrome (BLS). In this review, we discuss the agents that both induce and inhibit class II MHC expression, the function of class II MHC antigens with an emphasis on the ability of these proteins to act as signal transducing molecules, and the molecular regulation of class II MHC expression.
引用
收藏
页码:311 / 330
页数:20
相关论文
共 172 条
[1]   HOW ARE CLASS-II MHC GENES TURNED ON AND OFF [J].
ABDULKADIR, SA ;
ONO, SJ .
FASEB JOURNAL, 1995, 9 (14) :1429-1435
[2]  
ADBULKADIR SA, 1995, J EXP MED, V182, P487
[3]   CHARACTERIZATION OF A CIS-ACTING REGULATORY ELEMENT WHICH SILENCES EXPRESSION OF THE CLASS II-A BETA-GENE IN EPITHELIUM [J].
ALBERT, SE ;
STRUTZ, F ;
SHELTON, K ;
HAVERTY, T ;
SUN, MJ ;
LI, SR ;
DENHAM, A ;
MAKI, RA ;
NEILSON, EG .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (01) :233-240
[4]   MYCOPLASMA ARTHRITIDIS-DERIVED SUPERANTIGEN INDUCES PROINFLAMMATORY MONOKINE GENE-EXPRESSION IN THE THP-1 HUMAN MONOCYTIC CELL-LINE [J].
ALDACCAK, R ;
MEHINDATE, K ;
HEBERT, J ;
MECHERI, S ;
MOURAD, W ;
RINK, L .
INFECTION AND IMMUNITY, 1994, 62 (06) :2409-2416
[5]  
ANDERSSON G, 1990, J IMMUNOL, V145, P3456
[6]   AUTOCRINE SECRETION OF TUMOR NECROSIS FACTOR UNDER THE INFLUENCE OF INTERFERON-GAMMA AMPLIFIES HLA-DR GENE INDUCTION IN HUMAN-MONOCYTES [J].
ARENZANASEISDEDOS, F ;
MOGENSEN, SC ;
VUILLIER, F ;
FIERS, W ;
VIRELIZIER, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (16) :6087-6091
[7]  
BASTA PV, 1989, J IMMUNOL, V142, P2895
[8]   ROLE OF MHC GENE-PRODUCTS IN IMMUNE REGULATION [J].
BENACERRAF, B .
SCIENCE, 1981, 212 (4500) :1229-1238
[9]   CLASS-II-ANTIGEN-NEGATIVE PATIENT AND MUTANT B-CELL LINES REPRESENT AT LEAST 3, AND PROBABLY 4, DISTINCT GENETIC-DEFECTS DEFINED BY COMPLEMENTATION ANALYSIS [J].
BENICHOU, B ;
STROMINGER, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (10) :4285-4288
[10]  
BENOS DJ, 1994, J BIOL CHEM, V269, P13811