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. 2015 Aug 24;125(9):3430–3432. doi: 10.1172/JCI83823

Figure 1. pDCs contribute to HIV-1–induced ILC3 dysfunction and depletion.

Figure 1

HIV-1 infects and activates pDCs, which produce high levels of IFN-I within lymph tissues. While increased IFN-I upregulates CD95 expression and sensitizes tissue-resident ILC3s to CD95/FasL-mediated apoptosis, it also partially impairs IL-17a and IL-22 production by gut ILC3s. Thus, the numeral and functional impairment of ILC3s may lead to the loss of intestinal epithelial integrity, resulting in the release of bacteria and their products, such as LPS, into blood that in turn induce systematic activation. However, three key questions require future study: (a) What is the role of IFN-I in the induction of ILC3 apoptosis in vivo? (b) Do pDCs produce other cytokines involved in the regulation of ILC3? (c) How do human ILC3s protect against mucosal bacterial infections and maintain the mucosal barrier? The resolution of these issues will help determine whether strategies aimed to modulate ILC3 responses have therapeutic potential to benefit patients with chronic HIV-1.