Review series on helminths, immune modulation and the hygiene hypothesis: Mechanisms underlying helminth modulation of dendritic cell function

被引：70

作者：

Carvalho, Lucas

Sun, Jie ^{[2
]}

Kane, Colleen ^{[3
]}

Marshall, Fraser

Krawczyk, Connie ^{[4
]}

Pearce, Edward J. ^{[1
]}

机构：

[1] Univ Penn, Dept Pathobiol, Sch Vet Med, Philadelphia, PA 19104 USA

[2] Univ Virginia, Beirne B Carter Ctr Immunol Res, Charlottesville, VA USA

[3] Centocor Inc, Wayne, PA USA

[4] Merck Frosst Canada & Co Inc, Merck Res Labs, Kirkland, PQ, Canada

来源：

IMMUNOLOGY | 2009年 / 126卷 / 01期

关键词：

dendritic cell; helminth pathogens; immunoregulation; Toll-like receptors; T helper type 1 (Th1); Th2; MANSONI EGG ANTIGENS; ALLERGIC AIRWAY INFLAMMATION; NEGLECTED TROPICAL DISEASES; ACTIVATED PROTEIN-KINASE; TH2 RESPONSE INDUCTION; REGULATORY T-CELLS; LECTIN DC-SIGN; NF-KAPPA-B; IN-VIVO; CUTTING EDGE;

D O I：

10.1111/j.1365-2567.2008.03008.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：

Dendritic cells (DCs) play a central role in activating CD4 T (T helper, Th) cells. As a component of their response to pathogen-associated stimuli, DCs produce cytokines and express surface molecules that provide important cues to modulate the effector functions of responding Th cells. Much is known of how DCs respond to, and influence immune response outcome to, bacterial and viral pathogens. However, relatively little is understood about how DCs respond to helminth parasites. This is an area of considerable interest since it impacts our understanding of the initiation of Th2 responses, which are stereotypically associated with helminth infections, and the regulation of allergic and autoimmune pathologies which evidence suggests are less severe or absent in individuals infected with helminths. This review attempts to summarize our understanding of the effects of helminth products on dendritic cell biology.

引用

页码：28 / 34

页数：7

共 75 条

[1] Cutting edge: Different toll-like receptor agonists instruct dendritic cells to induce distinct th responses via differential modulation of extracellular signal-regulated kinase-mitogen-activated protein kinase and c-fos [J].