An enteric helminth infection protects against an allergic response to dietary antigen

被引:188
作者
Bashir, MEH
Andersen, P
Fuss, IJ
Shi, HN
Nagler-Anderson, C
机构
[1] Massachusetts Gen Hosp East, Mucosal Immunol Lab, Charlestown, MA 02129 USA
[2] Harvard Univ, Sch Med, Charlestown, MA 02129 USA
[3] NIH, Mucosal Immun Sect, Bethesda, MD 20892 USA
关键词
D O I
10.4049/jimmunol.169.6.3284
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Although helminths induce a polarized Th2 response they have been shown, in clinical studies, to confer protection against allergies. To elucidate the basis for this paradox, we have examined the influence of an enteric helminth infection on a model of food allergy. Upon Ag challenge, mice fed peanut (PN) extract plus the mucosal adjuvant cholera toxin (CT) produced PN-specific IgE that correlated with systemic anaphylactic symptoms and elevated plasma histamine. PN-specific IgE was not induced in helminth-infected mice fed PN without CT. Moreover, when PN plus CT was fed to helminth-infected mice, both PN-specific IgE and anaphylactic symptoms were greatly diminished. The down-regulation of PN-specific IgE was associated with a marked reduction in the secretion of IL-13 by PN-specific T cells. When helminth-infected PN plus CT-sensitized mice were treated with neutralizing Abs to IL-10, the PN-specific IgE response and anaphylactic symptoms were similar to, or greater than, those seen in mice that receive PN and CT alone. Taken together, these results suggest that helminth-dependent protection against allergic disease involves immunoregulatory mechanisms that block production of allergen-specific IgE.
引用
收藏
页码:3284 / 3292
页数:9
相关论文
共 36 条
[1]   Inhibition of human allergic T-cell responses by IL-10-treated dendritic cells: Differences from hydrocortisone-treated dendritic cells [J].
Bellinghausen, I ;
Brand, U ;
Steinbrink, K ;
Enk, AH ;
Knop, J ;
Saloga, J .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 108 (02) :242-249
[2]   Immune dysregulation in Ethiopian immigrants in Israel: Relevance to helminth infections? [J].
Bentwich, Z ;
Weisman, Z ;
Moroz, C ;
BarYehuda, S ;
Kalinkovich, A .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1996, 103 (02) :239-243
[3]   ANAPHYLACTIC REACTIONS AFTER GAMMA-GLOBULIN ADMINISTRATION IN PATIENTS WITH HYPOGAMMAGLOBULINEMIA - DETECTION OF IGE ANTIBODIES TO IGA [J].
BURKS, AW ;
SAMPSON, HA ;
BUCKLEY, RH .
NEW ENGLAND JOURNAL OF MEDICINE, 1986, 314 (09) :560-564
[4]  
Cong YZ, 1997, J IMMUNOL, V159, P5301
[5]   Immunology - Asthma: An epidemic in the absence of infection? [J].
Cookson, WOCM ;
Moffatt, MF .
SCIENCE, 1997, 275 (5296) :41-42
[6]   Regulatory activity of autocrine IL-10 on dendritic cell functions [J].
Corinti, S ;
Albanesi, C ;
la Sala, A ;
Pastore, S ;
Girolomoni, G .
JOURNAL OF IMMUNOLOGY, 2001, 166 (07) :4312-4318
[7]   Emerging immune targets for the therapy of allergic asthma [J].
Corry, DB .
NATURE REVIEWS DRUG DISCOVERY, 2002, 1 (01) :55-64
[8]   Antigen-specific cellular hyporesponsiveness in a chronic human helminth infection is mediated by Th3/Tr1-type cytokines IL-10 and transforming growth factor-β but not by a Th1 to Th2 shift [J].
Doetze, A ;
Satoguina, J ;
Burchard, G ;
Rau, T ;
Löliger, C ;
Fleischer, B ;
Hoerauf, A .
INTERNATIONAL IMMUNOLOGY, 2000, 12 (05) :623-630
[9]   Interleukin (IL)-4-independent induction of immunoglobulin (Ig)E, and perturbation of T cell development in transgenic mice expressing IL-13 [J].
Emson, CL ;
Bell, SE ;
Jones, A ;
Wisden, W ;
McKenzie, ANJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (02) :399-404
[10]   IL-13 overexpression predisposes to anaphylaxis following antigen sensitization [J].
Fallon, PG ;
Emson, CL ;
Smith, P ;
McKenzie, ANJ .
JOURNAL OF IMMUNOLOGY, 2001, 166 (04) :2712-2716