Plasmacytoid dendritic cells promote HIV-1–induced group 3 innate lymphoid cell depletion

Blocking type I interferon signaling enhances T cell recovery and reduces HIV-1 reservoirs

“…The higher levels of SIV infection probably lead to the accelerated disease progression during the late (43); thus the reduction may be due to the redistribution of HIV-1 reservoir cells to lymphoid organs induced by IFN-α. Interestingly, treatment of HIV-1/HCV-coinfected patients with IFN-α/ribavirin appears to lead to a significant reduction of both CD4 and CD8 T cells (18,20,21), which is consistent with our previous finding that IFN-I contributes to T cell depletion during chronic HIV-1 infection (28,44). In addition, a low level of HIV-1 replication in the presence of cART may also contribute to the HIV-1 reservoir pool (45).…”

A functional DC cross talk promotes human ILC homeostasis in humanized mice

“…A recent report showed that HIV-1 infection depletes human ILC3, thus providing a plausible mechanism for loss of intestinal homeostasis in the context of this disease. 20 Enhanced human ILC3 development in BRGSF HIS mice offers a means to study these cells in various viral inflammation conditions.…”

“…15 In contrast, reports on other human ILC subsets in humanized mice are scarce and only in the context of inflammation. 19,20 Several ILC subsets inhabit mucosal tissues, and the reconstitution of these sites in most humanized mouse models appears rather limited (reviewed in Ito et al 21 ). This may result from poor homing or maintenance of human hematopoietic cells because of incompatibilities in adhesion molecules, chemokine/chemokine receptors, and/or growth and survival factors.…”

The tragic fate of group 3 innate lymphoid cells during HIV-1 infection

“…However, due to the lack of a robust animal model, the causation and the underlying mechanism that link ILC3 depletion and HIV-1 pathogenesis are poorly understood. In this issue, Zhang and colleagues confirmed that ILC3s are depleted in both blood and gut tissues of HIV-1-infected patients and that this depletion correlates with HIV-1 disease progression (21). The authors developed a technique to further investigate how the number of ILC3s may influence HIV-1 pathogenesis.…”