Cytokines and beyond: Regulation of innate immune responses during helminth infection.

Cytokines and beyond: Regulation of innate immune responses during helminth infection.
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DOI:
10.1016/j.cyto.2018.08.021
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发表时间:
2020-09
期刊:
影响因子:
3.8
通讯作者:
Tait Wojno ED
Tait Wojno ED
中科院分区:
医学3区
文献类型:
--
作者:
Oyesola OO;Früh SP;Webb LM;Tait Wojno ED

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Parasitic helminth infection elicits a type 2 cytokine-mediated inflammatory response. During type 2 inflammation, damaged or stimulated epithelial cells exposed to helminths and their products produce alarmins and cytokines including IL-25, IL-33, and thymic stromal lymphopoietin. These factors promote innate immune cell activation that supports the polarization of CD4+ T helper type 2 (Th2) cells. Activated innate and Th2 cells produce the cytokines IL-4, −5, −9, and −13 that perpetuate immune activation and act back on the epithelium to drive goblet cell hyperplasia and increased epithelial cell turnover. Together, these events drive worm expulsion and wound healing processes. While the role of Th2 cells in this context has been heavily studied, recent work has revealed that epithelial cell-derived cytokines are drivers of key innate immune responses that are critical for type 2 anti-helminth responses. Cutting-edge studies have begun to fully assess how other factors and pathways, including lipid mediators, chemokines, Fc receptor signaling, danger-associated molecular pattern molecules, and direct cell-cell interactions, also participate in shaping innate cell-mediated type 2 inflammation. In this review, we discuss how these pathways intersect and synergize with pathways controlled by epithelial cell-derived cytokines to coordinate innate immune responses that drive helminth-induced type 2 inflammation.
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