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A surprising role for TLR7

Nature Immunology volume 16, pages 8–9 (2015)Cite this article

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Ligation of the Toll-like receptor TLR7 in human CD4+ T cells elicits an anergic state that may contribute to CD4+ T cell hyporesponsiveness after infection with human immunodeficiency virus type 1 and may also enhance propagation of this virus.

TLR7 is one of several Toll-like receptors (TLR3, TLR7, TLR8 and TLR9) that recognize microbial nucleic acid sequences. TLR7 and TLR8, which recognize single-stranded RNA, are distributed broadly among myeloid and other cells and are characteristically expressed in endosomal compartments, where their engagement with microbial sequences is thought to take place. In this issue of Nature Immunology, Dominguez-Villar et al. demonstrate a surprising role for TLR7 in host-virus relationships1. In a paper fraught with novelty, the authors provide evidence that engagement of TLR7 expressed in primary human CD4+ T cells can induce anergy. They also find that activation of a TLR7-dependent mechanism in CD4+ T cells promotes the replication of human immunodeficiency virus type 1 (HIV-1) within these cells—a hitherto unexpected role for this microbial sensor.

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Figure 1: The engagement of TLR7 in isolated CD4+ T cells induces an anergic state and promotes HIV-1 replication.

Marina Corral Spence/Nature Publishing Group

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  1. Michael M. Lederman is with Case Western Reserve University, University Hospitals Case Medical Center, Cleveland, Ohio, USA.

    Michael M Lederman

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  1. Michael M Lederman
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Correspondence to Michael M Lederman.

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Lederman, M. A surprising role for TLR7. Nat Immunol 16, 8–9 (2015). https://doi.org/10.1038/ni.3051

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