The viral reservoir of infected CD4+ T cells remains a barrier for effective therapeutic elimination of HIV. In June of 2017, an article in Nature showed that the FcÿRIIa (CD32a) is a marker for those CD4+ T cells that harbor replication competent HIV provirus (Nature, 543, 564-567, 2017). This discovery is considered as an important step in advancing the mechanistic approaches to eradicate HIV (Immunity, 46, 527-529, 2017).
It has been argued that the CD4+ T-cells do not express low affinity FcRs and these receptors do not have a role in CD4+ T cell function (Nat Rev Immunol, 8. 34-47, 2008; Immunol Rev 268, 25-51, 2015). We established the conditions under which CD4+ T cells express FcÿRIIIa and further defined their role in T cell receptor signaling and cellular differentiation (J of Biol Chem, 290, 5127-40, 2015; 291, 1368-86, 2016). ProGen Biologics have generated fluorescently labeled IC tag to identify those CD4+ T cells that express CD32a and/or CD16a.
An early study suggested that HIV induced CD4+ T cell depletion is dependent on the formation of immune complexes (ICs) that attach to CD4+ T cells (Immunology Letters, 76, 69-78, 2001)1. This study also found that the amount of IC bound circulating CD4+ lymphocytes correlate with the depletion of CD4+ T cells, while plasma viral load correlate to lymphocyte activation
To explore the utility of Fc-receptor expressing CD4+ T cells in HIV pathology and their role in anti-retroviral therapy, we offer a flow cytometry-based quantitation of these cells.
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Dr. Anil K. Chauhan