Bone Marrow CD34+ Progenitor Cells from HIV-Infected Patients Show an Impaired T Cell Differentiation Potential Related to Proinflammatory Cytokines

Veronica Bordoni; Michele Bibas; Domenico Viola; Alessandra Sacchi; Eleonora Cimini; Nicola Tumino; Rita Casetti; Alessandra Amendola; Adriana Ammassari; Chiara Agrati; Federico Martini

doi:10.1089/aid.2016.0195

Bone Marrow CD34⁺ Progenitor Cells from HIV-Infected Patients Show an Impaired T Cell Differentiation Potential Related to Proinflammatory Cytokines

Veronica Bordoni, Michele Bibas, Domenico Viola, Alessandra Sacchi, Eleonora Cimini, Nicola Tumino, Rita Casetti, Alessandra Amendola, Adriana Ammassari, Chiara Agrati, Federico Martini

Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani

Research output: Contribution to journal › Article › peer-review

Abstract

The impact of HIV infection on the frequency and differentiation capability of CD34⁺ bone marrow hematopoietic progenitor cells (BM-HPCs) is still debated, having a possible primary role in antiretroviral-induced immunoreconstitution. We investigated the influence of HIV replication or proinflammatory cytokines on lymphopoietic capability of BM-HPCs from seven viremic (VR) and five nonviremic (NVR) HIV-infected patients. We found that BM-HPCs from VR patients were unable to differentiate in vitro toward T cells, and produced proinflammatory cytokines in the absence of viral replication. In contrast, the lymphoid differentiation potential of BM-HPCs was partially restored in successfully antiretroviral therapy-treated patients. We also showed that TLR8 triggering induced BM-HPCs from healthy donors to release proinflammatory cytokines affecting T cell differentiation. These data suggest that in HIV-infected patients, the lymphopoiesis capability of BM-HPCs may be modulated by a virus-driven autocrine mechanism involving proinflammatory cytokines.

Original language	English
Pages (from-to)	590-596
Number of pages	7
Journal	AIDS Research and Human Retroviruses
Volume	33
Issue number	6
DOIs	https://doi.org/10.1089/aid.2016.0195
Publication status	Published - Jun 1 2017

Keywords

HIV
immune response
in vitro models
inflammation
T cells

ASJC Scopus subject areas

Immunology
Virology
Infectious Diseases

Access to Document

10.1089/aid.2016.0195

Cite this

Bordoni, V., Bibas, M., Viola, D., Sacchi, A., Cimini, E., Tumino, N., Casetti, R., Amendola, A., Ammassari, A., Agrati, C., & Martini, F. (2017). Bone Marrow CD34⁺ Progenitor Cells from HIV-Infected Patients Show an Impaired T Cell Differentiation Potential Related to Proinflammatory Cytokines. AIDS Research and Human Retroviruses, 33(6), 590-596. https://doi.org/10.1089/aid.2016.0195

Bordoni, V , Bibas, M, Viola, D, Sacchi, A , Cimini, E , Tumino, N , Casetti, R , Amendola, A , Ammassari, A , Agrati, C & Martini, F 2017, 'Bone Marrow CD34⁺ Progenitor Cells from HIV-Infected Patients Show an Impaired T Cell Differentiation Potential Related to Proinflammatory Cytokines', AIDS Research and Human Retroviruses, vol. 33, no. 6, pp. 590-596. https://doi.org/10.1089/aid.2016.0195

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abstract = "The impact of HIV infection on the frequency and differentiation capability of CD34+ bone marrow hematopoietic progenitor cells (BM-HPCs) is still debated, having a possible primary role in antiretroviral-induced immunoreconstitution. We investigated the influence of HIV replication or proinflammatory cytokines on lymphopoietic capability of BM-HPCs from seven viremic (VR) and five nonviremic (NVR) HIV-infected patients. We found that BM-HPCs from VR patients were unable to differentiate in vitro toward T cells, and produced proinflammatory cytokines in the absence of viral replication. In contrast, the lymphoid differentiation potential of BM-HPCs was partially restored in successfully antiretroviral therapy-treated patients. We also showed that TLR8 triggering induced BM-HPCs from healthy donors to release proinflammatory cytokines affecting T cell differentiation. These data suggest that in HIV-infected patients, the lymphopoiesis capability of BM-HPCs may be modulated by a virus-driven autocrine mechanism involving proinflammatory cytokines.",

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