Immunophenotypic characterization of T-cell receptor γδ T cells and mucosal-associated invariant cells in HIV-infected individuals developing Hodgkin’s lymphoma. Infectious Agents and Cancer
T-cell receptor (TCR) γδ cells and/or mucosal-associated invariant T (MAIT) cells might be associated with the increased risk of non-AIDS defining cancers (NADCs) because both serve as a link between the adaptive and the innate immune system and exert direct anti-viral and anti-tumor activity.
Muller et al. hypothesized that the extent of depletion and/or phenotype of MAIT and TCR γδ cell differ between HIV-infected patients developing Hodgkin’s lymphoma (HL) (prior to the diagnosis of HL) and HIV-infected matched controls. To address this possibility, they performed a detailed phenotypic characterization of TCR γδ and MAIT cells in the PB of HIV-infected individuals enrolled in the Swiss HIV Cohort Study (SHCS).
The authors used cryopreserved PBMCs of HIV-infected individuals developing HL, matched HIV-infected controls without (w/o) HL and healthy controls for immunophenotyping by polychromatic flow cytometry, including markers for activation, exhaustion and chemokine receptors.
They identified significant differences in the CD4+ T cell count between HIV-infected individuals developing HL and HIV-infected matched controls within 1 year before cancer diagnosis. They also observed substantial differences in the cellular phenotype mainly between healthy controls and HIV infection irrespective of HL. A number of markers tended to be different in Vδ1 and MAIT cells in HIV+HL+ patients vs. HIV+ w/o HL patients; notably, they observed significant differences for the expression of CCR5, CCR6 and CD16 between these two groups of HIV+ patients.
In conclusion, this study provides additional evidence for the ambiguous lower CD4+ cell counts just prior to HL as compared to their matched controls even though patients were treated successfully with combination antiretroviral therapy. These results showed subtle differences between populations of TCR γδ and MAIT cells in HIV+-patients with vs. without HL. To what extent these subtle differences contribute to the pathogenesis of HL remains unknown. Future studies need to address their potential role in the development of NADCs in HIV-infected individuals, and whether they might be exploited in novel types of cell therapy.