{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T17:32:03Z","timestamp":1776274323189,"version":"3.50.1"},"reference-count":75,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2021,12,22]],"date-time":"2021-12-22T00:00:00Z","timestamp":1640131200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01NS066842"],"award-info":[{"award-number":["R01NS066842"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["U01-AI35042"],"award-info":[{"award-number":["U01-AI35042"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["T32AI007540"],"award-info":[{"award-number":["T32AI007540"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathogens"],"abstract":"<jats:p>CD4+ CCR6+ T cells are highly susceptible to HIV infection, and a high cytokine producing CCR6+ T cell subset is selectively lost during HIV infection. The CCR6 chemokine MIP-3\u03b1 (CCL20) is produced at sites of infection in SIV animal models. Recently, we have shown that MIP-3\u03b1 inhibits HIV replication. This inhibition of HIV infection is mediated by CCR6 signaling and eventuates in increased APOBEC3G expression. Since there are few existing reports on the role of MIP-3\u03b1 in health or disease, we studied its production by PBMCs from HIV-seronegative and HIV+ subjects. We evaluated the ability of PBMCs to produce MIP-3\u03b1 in response to antigen stimulation using cells obtained from two groups: one composed of HIV-seronegative subjects (n = 16) and the other composed of HIV+ subjects (n = 58), some asymptomatic and some with clinically defined AIDS. Antigens included fragment C of the tetanus toxin, Candida albicans, whole-inactivated HIV, and HIV p24. MIP-3\u03b1 was detected by ELISA in tissue culture supernatants of antigen-stimulated PBMCs. MIP-3\u03b1 production by antigen-stimulated PBMCs was readily measured for HIV-negative subjects and for HIV-seropositive asymptomatic subjects, but not for patients with AIDS. These results suggest that subversion of the MIP-3\u03b1-CCR6 axis by HIV during the course of infection contributes to the loss of immune function that eventually leads to AIDS.<\/jats:p>","DOI":"10.3390\/pathogens11010007","type":"journal-article","created":{"date-parts":[[2021,12,23]],"date-time":"2021-12-23T02:01:19Z","timestamp":1640224879000},"page":"7","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Decreased MIP-3\u03b1 Production from Antigen-Activated PBMCs in Symptomatic HIV-Infected Subjects"],"prefix":"10.3390","volume":"11","author":[{"given":"Fuchun","family":"Zhang","sequence":"first","affiliation":[{"name":"Laboratory of Virus-Host Interactions, Division of Virology, Pathogenesis, and Cancer, Institute of Human Virology, Department of Microbiology and Immunology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA"},{"name":"Department of Infectious Diseases, Guangzhou No. 8 People\u2019s Hospital, Guangzhou Medical College, Guangzhou 510060, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lingling","family":"Sun","sequence":"additional","affiliation":[{"name":"Laboratory of Virus-Host Interactions, Division of Virology, Pathogenesis, and Cancer, Institute of Human Virology, Department of Microbiology and Immunology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark K.","family":"Lafferty","sequence":"additional","affiliation":[{"name":"Laboratory of Virus-Host Interactions, Division of Virology, Pathogenesis, and Cancer, Institute of Human Virology, Department of Microbiology and Immunology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph B.","family":"Margolick","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4095-6950","authenticated-orcid":false,"given":"Alfredo","family":"Garzino-Demo","sequence":"additional","affiliation":[{"name":"Laboratory of Virus-Host Interactions, Division of Virology, Pathogenesis, and Cancer, Institute of Human Virology, Department of Microbiology and Immunology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA"},{"name":"Department of Molecular Medicine, University of Padova, 35121 Padova, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,12,22]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"243","DOI":"10.1023\/A:1027329721892","article-title":"Chemokine Receptors and Chemokines in HIV Infection","volume":"18","author":"DeVico","year":"1998","journal-title":"J. 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