Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6139099 | Virology | 2015 | 10 Pages |
Abstract
Exosomes are extracellular vesicles (EVs) that play a role in intercellular communication. Stimulation of dendritic cells by the HIV-1 virus triggers their release. HIV-1 binds to dendritic cells via dendritic cell immunoreceptor (DCIR). This study shows that inhibiting the binding to DCIR significantly decreases exosome release by HIV-1-pulsed dendritic cells. In addition, exosome release from Raji-CD4 expressing DCIR cells stimulated by anti-DCIR or HIV-1 is decreased when the immunoreceptor tyrosine-based inhibition motif (ITIM) signaling motif of DCIR is mutated. Unlike the EVs released from Raji-CD4-DCIR cells after antibody stimulation, those released from HIV-1-infected cells contain the pro-apoptotic protein DAP-3. Furthermore, EVs from HIV-1 pulsed dendritic cells increase spontaneous apoptosis in uninfected CD4 T lymphocytes while they decrease it in neutrophils. This study describes for the first time that DCIR plays a role in the release of exosomes strengthening the importance of this receptor and EVs/exosomes in HIV-1 pathogenesis.
Keywords
CD4 T lymphocytedendritic cell immunoreceptorCD4 T lymphocytesDCIRDC-SIGNITIMMTTAChEAcetylcholinesteraseExosomesAIDSimmunoreceptor tyrosine-based inhibition motifbradykininThiazolyl blue tetrazolium bromideExtracellular vesiclesApoptosisDendritic cellsDendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrinNeutrophilsHIV-1
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Authors
Claude M. Mfunyi, Myriam Vaillancourt, Julien Vitry, Thy-René Nsimba Batomene, Alma Posvandzic, Alexandra A. Lambert, Caroline Gilbert,