Complement receptors regulate lipopolysaccharide-induced T-cell stimulation

被引:19
作者
Kaya, Z
Tretter, T
Schlichting, J
Leuschner, F
Afanasyeva, M
Katus, HA
Rose, NR
机构
[1] Univ Heidelberg, Dept Internal Med 3, D-69120 Heidelberg, Germany
[2] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21205 USA
[3] Johns Hopkins Med Inst, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA
[4] Johns Hopkins Med Inst, Dept Mol Biol & Genet, Baltimore, MD 21205 USA
关键词
T lymphocytes; lipopolysaccharide; complement; cell surface molecules; cellular activation;
D O I
10.1111/j.1365-2567.2004.02113.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Complement receptors type 1 and 2 (CR1 (CD35)/CR2 (CD21)) are known to enhance the adaptive immune response. In mice, CR1/CR2 are expressed on B cells, follicular dendritic cells, and activated granulocytes. Recently, we showed that a subset of CD44(high) and CD62L(low) T cells also expresses CR1 and CR2. We now report that CR1/CR2 are detectable on both CD4(+) and CD8(+) subsets of T cells. Lipopolysaccharide (LPS) from Gram-negative bacteria causes polyclonal activation of B cells and stimulation of macrophages and other antigen-presenting cells. We further demonstrate that LPS induced marked up-regulation of CD25 and CD69 on T cells from CR1/CR2 sufficient (Cr+/+), but significantly lower up-regulation on T cells from CR1/CR2 deficient (Cr-/-) mice. These findings point to a novel mechanism by which CR1/CR2 modulates the activation of T cells by LPS.
引用
收藏
页码:493 / 498
页数:6
相关论文
共 24 条
[11]   A further link between innate and adaptive immunity:: C3 deposition on antigen-presenting cells enhances the proliferation of antigen-specific T cells [J].
Kerekes, K ;
Prechl, J ;
Bajtay, Z ;
Józsi, M ;
Erdei, A .
INTERNATIONAL IMMUNOLOGY, 1998, 10 (12) :1923-1930
[12]  
KINOSHITA T, 1988, J IMMUNOL, V140, P3066
[13]   LPS PROMOTES CB3-INDUCED MYOCARDITIS IN RESISTANT B10.A MICE [J].
LANE, JR ;
NEUMANN, DA ;
LAFONDWALKER, A ;
HERSKOWITZ, A ;
ROSE, NR .
CELLULAR IMMUNOLOGY, 1991, 136 (01) :219-233
[14]  
Mattern T, 1998, J IMMUNOL, V160, P3412
[15]   B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells [J].
Moir, S ;
Malaspina, A ;
Li, YX ;
Chun, TW ;
Lowe, T ;
Adelsberger, J ;
Baseler, M ;
Ehler, LA ;
Liu, SY ;
Davey, RT ;
Mican, JAM ;
Fauci, AS .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (05) :637-645
[16]   Markedly impaired humoral immune response in mice deficient in complement receptors 1 and 2 [J].
Molina, H ;
Holers, VM ;
Li, B ;
Fang, YF ;
Mariathasan, S ;
Goellner, J ;
StraussSchoenberger, J ;
Karr, RW ;
Chaplin, DD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (08) :3357-3361
[17]  
PERUSSIA B, 1992, J IMMUNOL, V149, P3495
[18]   CACHECTIN TUMOR NECROSIS FACTOR EXERTS ENDOCRINE, PARACRINE, AND AUTOCRINE CONTROL OF INFLAMMATORY RESPONSES [J].
SHERRY, B ;
CERAMI, A .
JOURNAL OF CELL BIOLOGY, 1988, 107 (04) :1269-1277
[19]   Type I interferon-mediated stimulation of T cells by CgG DNA [J].
Sun, SQ ;
Zhang, XH ;
Tough, DF ;
Sprent, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (12) :2335-2342
[20]   T cell stimulation in vivo by lipopolysaccharide (LPS) [J].
Tough, DF ;
Sun, SQ ;
Sprent, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (12) :2089-2094