Abstract:
:HIV infection is associated with chronic inflammation in both non-treated and treated patients. TLR-dependent mechanisms are strongly involved in the maintenance of this inflammation. Indeed, the residual replication of HIV, the potential viral co-infections, or the products issued from microbial translocation provide TLR ligands, which contribute to trigger innate immune responses. Maintaining this chronic inflammation leads to an exhaustion of the immune system. Therefore, the TLR-dependent responses could be altered in HIV-infected patients. To investigate this hypothesis, we performed high-resolution phenotyping using a mass cytometry panel of 34 cell markers. Whole blood cells from healthy, non-treated HIV-infected and ART-treated HIV-infected subjects were stimulated with LPS, R848 or Poly(I:C). We observed the immune responses induced in T-cells, B-cells, polymorphonuclear cells, NK cells, basophils, monocytes and dendritic cells. We observed that, for either LPS or R848 stimulations, the production of cytokines in monocytes and conventional dendritic cells was delayed in treated or non-treated HIV-infected patients, compared to healthy individuals. These results suggest that leukocytes from chronic HIV-infected patients are slower to respond following the sensing of pathogens and danger signals, which may be an important feature of HIV infection.
journal_name
Cytokinejournal_title
Cytokineauthors
Leite Pereira A,Tchitchek N,Marcos Lopez E,Lambotte O,Le Grand R,Cosma Adoi
10.1016/j.cyto.2018.08.018subject
Has Abstractpub_date
2018-11-01 00:00:00pages
97-105eissn
1043-4666issn
1096-0023pii
S1043-4666(18)30353-3journal_volume
111pub_type
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