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Published on: January 5, 2016
Increased extrafollicular expression of the B-cell stimulatory molecule CD70 in HIV-1-infected individuals
Rebecka Lantto1, Aikaterini Nasi, Stefano Sammicheli
1aDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden bDynamics of Immune Responses, Division of Immunology, San Raffaele Scientific Institute, Milan, Italy cLaboratory of Retrovirology, Department of infection and immunity, Luxembourg Institute of Health, Luxembourg dImmunology and Infectious Diseases, GIGA-Signal Transduction, University of Liège, Liege, Belgium eDepartment of Infectious Diseases/Venhälsan, South General Hospital, Stockholm, Sweden.
Objective:
CD70 molecules expressed by activated T cells provide potent B cell stimulatory signals. We hypothesized that an altered CD70 expression might contribute to B cell abnormalities during HIV-1 infection.
Design:
CD70 expression and the functional and migratory properties of the CD4CD70 T lymphocytes were analyzed in HIV-1-infected patients and in humanized mice. Correlations were tested between CD70 expression and features of B-cell activation, apoptosis sensitivity and functional exhaustion.
Methods:
CD4CD70 T cells were analyzed in cohorts of CD4 T-cell lymphopenic, viremic or nonlymphopenic, nonviremic HIV-1-infected patients and in noninfected individuals. CD70 upregulation was also followed in HIV-1-infected humanized mice. CD38, CD95, LAIR1 and PD-1 expressions were monitored on B-cell subpopulations, Ki67 was assessed to estimate B-cell proliferation and antibody levels were measured in plasma.
Results:
Blood CD4CD70 T-cell frequencies increased in response to CD4 T-cell depletion or high viremia levels as a possible consequence of increased activation and proliferation in this subset. CD4CD70 T cells produced T-helper 1-type cytokines and expressed chemokine receptors mobilizing toward sites of inflammation but not to lymphoid follicles. High CD70 expression was observed in HIV-1-infected humanized mice at extrafollicular sites (peritoneum, bone-marrow). CD4CD70 T-cell frequencies correlated with the expression of the activation marker CD38 and the death receptor CD95 on various memory B-cell subsets, with B-cell proliferation and with plasma IgG levels.
Conclusions:
CD4CD70 T cells may contribute to B cell hyperactivation and accelerated memory B-cell turnover during HIV-1 infection.
