Journal
NATURE IMMUNOLOGY
Volume 10, Issue 9, Pages 1008-U106Publisher
NATURE RESEARCH
DOI: 10.1038/ni.1753
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Funding
- US National Institutes of Health [AI07621, R01 AI057653, R01 AI057653-S1, R01 AI074378]
- Irma T. Hirschl Charitable Trust
- Cornell Comprehensive Cancer Center
- Ministerio de Ciencia e Innovacion
- Desarollo e Innovacion Tecnologica [SAF 2008-02725]
- Cancer Research Institute
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007621, R01AI074378, R01AI057653] Funding Source: NIH RePORTER
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Contact-dependent communication between immune cells generates protection but also facilitates viral spread. Here we found that macrophages formed long-range actin-propelled conduits in response to negative factor (Nef), a human immunodeficiency virus type 1 (HIV-1) protein with immunosuppressive functions. Conduits attenuated immunoglobulin G2 (IgG2) and IgA class switching in systemic and intestinal lymphoid follicles by shuttling Nef from infected macrophages to B cells through a guanine-exchange factor-dependent pathway involving the amino-terminal anchor, central core and carboxy-terminal flexible loop of Nef. By showing stronger virus-specific IgG2 and IgA responses in patients with Nef-deficient virions, our data suggest that HIV-1 exploits intercellular 'highways' as a 'Trojan horse' to deliver Nef to B cells and evade humoral immunity systemically and at mucosal sites of entry.
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