Chronic intestinal inflammatory condition generates IL-10-producing regulatory B cell subset characterized by CD1d upregulation

被引:805
作者
Mizoguchi, A [1 ]
Mizoguchi, E
Takedatsu, H
Blumberg, RS
Bhan, AK
机构
[1] Massachusetts Gen Hosp, Dept Pathol, Immunopathol Unit, Boston, MA 02114 USA
[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
[4] Brigham & Womens Hosp, Dept Med, Div Gastroenterol, Boston, MA 02115 USA
[5] Massachusetts Gen Hosp, Ctr Stusy Inflammatory Bowel Dis, Boston, MA 02114 USA
关键词
D O I
10.1016/S1074-7613(02)00274-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
B cells possess a variety of immune functions that are involved in normal and abnormal immune responses, including autoimmune disorders. Through murine models of intestinal inflammation, we here demonstrate a B cell subset that is induced in gut-associated lymphoid tissues and is characterized by CD1d upregulation. This B cell subset appears under a chronic inflammatory environment, produces IL-10, and suppresses progression of intestinal inflammation by downregulating inflammatory cascades associated with IL-1 upregulation and STAT3 activation rather than by altering polarized T helper responses. This study indicates that B cells, by producing cytokines such as IL-10, can act as regulatory cells in immunologically mediated inflammatory reactions.
引用
收藏
页码:219 / 230
页数:12
相关论文
共 58 条
[11]   Animal models of mucosal inflammation and their relation to human inflammatory bowel disease [J].
Blumberg, RS ;
Saubermann, LJ ;
Strober, W .
CURRENT OPINION IN IMMUNOLOGY, 1999, 11 (06) :648-656
[12]  
BLUMBERG RS, 1991, J IMMUNOL, V147, P2518
[13]  
Brossay L, 1997, J IMMUNOL, V159, P1216
[14]   CD1-mediated immune responses to glycolipids [J].
Burdin, N ;
Kronenberg, M .
CURRENT OPINION IN IMMUNOLOGY, 1999, 11 (03) :326-331
[15]   Interleukins 4 and 13 increase intestinal epithelial permeability by a phosphatidylinositol 3-kinase pathway - Lack of evidence for STAT 6 involvement [J].
Ceponis, PJM ;
Botelho, F ;
Richards, CD ;
McKay, DM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (37) :29132-29137
[16]   REGULATORY T-CELL CLONES INDUCED BY ORAL TOLERANCE - SUPPRESSION OF AUTOIMMUNE ENCEPHALOMYELITIS [J].
CHEN, YH ;
KUCHROO, VK ;
INOBE, J ;
HAFLER, DA ;
WEINER, HL .
SCIENCE, 1994, 265 (5176) :1237-1240
[17]   Ligation of intestinal epithelial CD1d induces bioactive IL-10: Critical role of the cytoplasmic tail in autocrine signaling [J].
Colgan, SP ;
Hershberg, RM ;
Furuta, GT ;
Blumberg, RS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (24) :13938-13943
[18]   T regulatory cells 1 inhibit a Th2-specific response in vivo [J].
Cottrez, F ;
Hurst, SD ;
Coffman, RL ;
Groux, H .
JOURNAL OF IMMUNOLOGY, 2000, 165 (09) :4848-4853
[19]   Involvement of CD1 in peripheral deletion of T lymphocytes is independent of NK T cells [J].
Dao, T ;
Exley, M ;
Mehal, WZ ;
Tahir, SMA ;
Snapper, S ;
Taniguchi, M ;
Balk, SP ;
Crispe, IN .
JOURNAL OF IMMUNOLOGY, 2001, 166 (05) :3090-3097
[20]   T helper cell 1-type CD4(+) T cells, but not B cells, mediate colitis in interleukin 10-deficient mice [J].
Davidson, NJ ;
Leach, MW ;
Fort, MM ;
ThompsonSnipes, L ;
Kuhn, R ;
Muller, W ;
Berg, DJ ;
Rennick, DM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (01) :241-251