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Diversity and dialogue in immunity to helminths

Identifieur interne : 000256 ( Istex/Corpus ); précédent : 000255; suivant : 000257

Diversity and dialogue in immunity to helminths

Auteurs : Judith E. Allen ; Rick M. Maizels

Source :

RBID : ISTEX:05917678AE415849C1BA2DDF7F6E8019BEB90474

Abstract

The vertebrate immune system has evolved in concert with a broad range of infectious agents, including ubiquitous helminth (worm) parasites. The constant pressure of helminth infections has been a powerful force in shaping not only how immunity is initiated and maintained, but also how the body self-regulates and controls untoward immune responses to minimize overall harm. In this Review, we discuss recent advances in defining the immune cell types and molecules that are mobilized in response to helminth infection. Finally, we more broadly consider how these immunological players are blended and regulated in order to accommodate persistent infection or to mount a vigorous protective response and achieve sterile immunity.

Url:
DOI: 10.1038/nri2992

Links to Exploration step

ISTEX:05917678AE415849C1BA2DDF7F6E8019BEB90474

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T helper 2 (T
<sub>H</sub>
2) cell, which produces a broad range of cytokines, including interleukin-4 (IL-4) and IL-13, which act on target cells expressing the IL-4 receptor α-chain. Target cells include most cells of the immune system but also local tissue cells such as epithelial cells that line mucosal surfaces.</li>
<li>Cells of the innate immune system, such as the recently described 'innate helper cells', can also produce type 2 cytokines. These cells function as effectors during the early stages of infection, but additionally create an environment that favours the induction of T
<sub>H</sub>
2-type responses.</li>
<li>T
<sub>H</sub>
2-type responses are initiated by alarm signals from epithelial cells, as well as by specific recognition of helminth products. A strict requirement for dendritic cells in this process has been established.</li>
<li>In addition to killing or expelling helminth parasites, type 2 immune responses contribute to rapid tissue repair, and this sometimes leads to fibrosis-related pathology. Many facets of type 2 immunity are consistent with evolutionary origins in wound-healing pathways, a reflection of the capacity of helminth parasites to damage tissue through migration and feeding.</li>
<li>T cell dynamics change over time, and T
<sub>H</sub>
2-type responses often decline during chronic helminth infection. Regulatory pathways, including regulatory T cells, restrain pathology and immune responses during infection, and some helminths are able to actively induce the expansion of regulatory populations.</li>
<li>Because mammals evolved in the presence of chronic infection, their immune systems may have compensated for the immune dampening effects of helminths. If so, over-reactive responses to innocuous antigens in the absence of infection may contribute to autoimmune disease and allergy.</li>
</list>
</p>
</execsumm>
<websumm>Exciting new studies have uncovered many of the molecules and cell types that contribute to 'type 2' immune responses. Here, Judith Allen and Rick Maizels discuss how these responses are generated and provide protective immunity during helminth infection.</websumm>
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<p>The vertebrate immune system has evolved in concert with a broad range of infectious agents, including ubiquitous helminth (worm) parasites. The constant pressure of helminth infections has been a powerful force in shaping not only how immunity is initiated and maintained, but also how the body self-regulates and controls untoward immune responses to minimize overall harm. In this Review, we discuss recent advances in defining the immune cell types and molecules that are mobilized in response to helminth infection. Finally, we more broadly consider how these immunological players are blended and regulated in order to accommodate persistent infection or to mount a vigorous protective response and achieve sterile immunity.</p>
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<title>Diversity and dialogue in immunity to helminths</title>
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<description>Judith E. Allen received her Ph.D. from the University of California, Berkeley, USA, and is currently Professor of Immunobiology at the University of Edinburgh, UK. Her laboratory uses helminth, allergy and wound repair models to understand the 'type 2' immune response in both evolutionary and practical terms with a particular interest in macrophage biology.</description>
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<description>Rick M. Maizels received his Ph.D. in immunology at the Medical Research Council National Institute for Medical Research (NIMR), Mill Hill, London, UK, and after postdoctoral research at the California Institute of Technology, University of California, Los Angeles, USA, and again at NIMR, moved to Imperial College London, UK, in 1983, where he was appointed Professor of Parasite Immunology in 1993. He took the Chair of Zoology at the University of Edinburgh in 1995. His laboratory combines cellular immunology studies on parasite infections with molecular studies of parasite-based immunosuppression in systems such as airway allergy.</description>
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<abstract lang="eng">The vertebrate immune system has evolved in concert with a broad range of infectious agents, including ubiquitous helminth (worm) parasites. The constant pressure of helminth infections has been a powerful force in shaping not only how immunity is initiated and maintained, but also how the body self-regulates and controls untoward immune responses to minimize overall harm. In this Review, we discuss recent advances in defining the immune cell types and molecules that are mobilized in response to helminth infection. Finally, we more broadly consider how these immunological players are blended and regulated in order to accommodate persistent infection or to mount a vigorous protective response and achieve sterile immunity.</abstract>
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