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Background:  Human Immunodeficiency Virus 1 (HIV-1) and  Mycobacterium Tuberculosis  (Mtb) co-infected patients are commonly at risk of immune reconstitution inflammatory syndrome (IRIS) when initiating antiretroviral treatment (ART). Evidence indicates that innate immunity plays a role in TB-IRIS. Here, we evaluate the phenotype of Gamma-delta (γδ) T cells and invariant Natural Killer (iNK) T cells in tuberculosis-associated IRIS.   Methods:  Forty-eight HIV+/TB+ patients (21 IRIS) and three control groups: HIV–/TB– (HD,  n  = 11), HIV+/TB– ( n  = 26), and HIV–/TB+ ( n  = 22) were studied. Samples were taken at ART initiation (week 2 of anti-tuberculosis treatment) and at the diagnosis of IRIS for HIV+/TB+; before ART for HIV+/TB-, and at week 2 of anti-tuberculosis treatment for HIV–/TB+ patients. γδ T cells and Invariant natural killer T (iNKT) cells were analyzed by flow cytometry.   Results:  Before ART, IRIS, and non-IRIS patients showed a similar proportion of γδ pos  T and iNKT cells. HLA-DR on γδ pos  T cells and δ2 pos γδ pos  T cells was significantly higher in TB-IRIS vs. non-IRIS patients and controls ( p  < 0.0001). NKG2D expression on γδ pos  T cells and the δ2 pos γδ pos  T cell subset was lower in HIV+/TB+ patients than controls. CD158a expression on γδ pos  T cells was higher in TB-IRIS than non-IRIS ( p  = 0.02), HIV+/TB–, and HIV–/TB- patients.   Conclusion:  The higher activation of γδ pos T cells and the γδ2 pos γδ pos  T cell subset suggests that γδ T cells may play a role in the pathogenesis of TB-IRIS.

frontiers in immunology

High Activation of γδ T Cells and the γδ2pos T-Cell Subset Is Associated With the Onset of Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome, ANRS 12153 CAPRI NK