Cutting edge:: B cells promote CD8+ T cell activation in MRL-Faslpr mice independently of MHC class I antigen presentation

被引:29
作者
Chan, OTM
Shlomchik, MJ
机构
[1] Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA
关键词
D O I
10.4049/jimmunol.164.4.1658
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Spontaneous CD8(+) T cell activation in MRL-Fas(lpr) mice is B cell dependent. It is unclear whether this B dependent activation is mediated by direct Ag presentation via MHC class I proteins (i.e., cross-presentation) or whether activation occurs by an indirect mechanism, e.g., via effects on CD4(+) cells. To determine how CD8(+) T cell activation is promoted by B cells, we created mixed bone marrow chimeras where direct MHC class I Ag presentation by B cells was abrogated while other leukocyte compartments could express MHC class I. Surprisingly, despite the absence of B cell class I-restricted Ag presentation, CD8+ T cell activation was intact in the chimeric mice. Therefore, the spontaneous B cell-dependent CD8(+) T cell activation that occurs in systemic autoimmunity is not due to direct presentation by B cells to CD8(+) T cells.
引用
收藏
页码:1658 / 1662
页数:5
相关论文
共 35 条
[21]   Mechanisms of T cell-induced glomerular injury in anti-glomeruler basement membrane (GBM) glomerulonephritis in rats [J].
Huang, XR ;
Tipping, PG ;
Apostolopoulos, J ;
Oettinger, C ;
DSouza, M ;
Milton, G ;
Holdsworth, SR .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1997, 109 (01) :134-142
[22]   Antigens varying in affinity for the B cell receptor induce differential B lymphocyte responses [J].
Kouskoff, V ;
Famiglietti, S ;
Lacaud, G ;
Lang, P ;
Rider, JE ;
Kay, BK ;
Cambier, JC ;
Nemazee, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (08) :1453-1464
[23]   ANTIGEN-SPECIFIC INTERACTION BETWEEN T-CELLS AND B-CELLS [J].
LANZAVECCHIA, A .
NATURE, 1985, 314 (6011) :537-539
[24]   Role of T cells in the mediation of heymann nephritis .2. Identification of th1 and cytotoxic cells in glomeruli [J].
Penny, MJ ;
Boyd, RA ;
Hall, BM .
KIDNEY INTERNATIONAL, 1997, 51 (04) :1059-1068
[25]  
RAULET DH, 1994, ADV IMMUNOL, V55, P381
[26]   A conditioned dendritic cell can be a temporal bridge between a CD4+ T-helper and a T-killer cell [J].
Ridge, JP ;
Di Rosa, F ;
Matzinger, P .
NATURE, 1998, 393 (6684) :474-478
[27]  
SCHULTZ KR, 1995, BONE MARROW TRANSPL, V16, P289
[28]   B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: Analysis of a new ''speed congenic'' stock of NOD.Ig mu(null) mice [J].
Serreze, DV ;
Chapman, HD ;
Varnum, DS ;
Hanson, MS ;
Reifsnyder, PC ;
Richard, SD ;
Fleming, SA ;
Leiter, EH ;
Shultz, LD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (05) :2049-2053
[29]   A RHEUMATOID-FACTOR TRANSGENIC MOUSE MODEL OF AUTOANTIBODY REGULATION [J].
SHLOMCHIK, MJ ;
ZHARHARY, D ;
SAUNDERS, T ;
CAMPER, SA ;
WEIGERT, MG .
INTERNATIONAL IMMUNOLOGY, 1993, 5 (10) :1329-1341
[30]  
Shustov A, 1998, J IMMUNOL, V161, P2848