TGF-beta and IL-10 production by HIV-specific CD8+ T cells is regulated by CTLA-4 signaling on CD4+ T cells
Immune dysregulation in HIV-1 infection is associated with increased expression of inhibitory molecules such as CTLA-4, TGF-beta, and IL-10. In this study we examined one potential mechanism for regulating TGF-beta and IL-10 expression by HIV-specific suppressor CD8+ T cells. No overlap between TGF-...
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| Veröffentlicht in: | PloS one 2009-12, Vol.4 (12), p.e8194-e8194 |
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| creator | Elrefaei, Mohamed Burke, Candace M Baker, Chris A R Jones, Norman G Bousheri, Stephanie Bangsberg, David R Cao, Huyen |
| description | Immune dysregulation in HIV-1 infection is associated with increased expression of inhibitory molecules such as CTLA-4, TGF-beta, and IL-10. In this study we examined one potential mechanism for regulating TGF-beta and IL-10 expression by HIV-specific suppressor CD8+ T cells. No overlap between TGF-beta, IL-10, and IFN-gamma cytokine production by HIV-specific CD8+ T cells was observed. TGF-beta positive and IL-10 positive cells were FOXP3 negative, CD25 negative, and displayed a heterogeneous surface expression of CD127. TGF-beta and IL-10 positive CD8+ T cells did not express CTLA-4. Nevertheless, CTLA-4 blockade resulted in a significant decrease in HIV-specific TGF-beta positive and IL-10 positive CD8+ T cell responses, and a concomitant increase in HIV-specific IFN-gamma positive CD8+ T cell responses. Depletion of CD4+ T cells abrogated the impact of CTLA-4 on HIV-specific TGF-beta positive and IL-10 positive CD8+ T cells. Our study suggests that CTLA-4 Signaling on CD4+ T cells regulates the inhibitory functions of the HIV-specific suppressor CD8+ T cells. |
| doi_str_mv | 10.1371/journal.pone.0008194 |
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In this study we examined one potential mechanism for regulating TGF-beta and IL-10 expression by HIV-specific suppressor CD8+ T cells. No overlap between TGF-beta, IL-10, and IFN-gamma cytokine production by HIV-specific CD8+ T cells was observed. TGF-beta positive and IL-10 positive cells were FOXP3 negative, CD25 negative, and displayed a heterogeneous surface expression of CD127. TGF-beta and IL-10 positive CD8+ T cells did not express CTLA-4. Nevertheless, CTLA-4 blockade resulted in a significant decrease in HIV-specific TGF-beta positive and IL-10 positive CD8+ T cell responses, and a concomitant increase in HIV-specific IFN-gamma positive CD8+ T cell responses. Depletion of CD4+ T cells abrogated the impact of CTLA-4 on HIV-specific TGF-beta positive and IL-10 positive CD8+ T cells. Our study suggests that CTLA-4 Signaling on CD4+ T cells regulates the inhibitory functions of the HIV-specific suppressor CD8+ T cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0008194</identifier><identifier>PMID: 20016783</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acquired immune deficiency syndrome ; AIDS ; Antigens ; Antigens, CD - immunology ; CD25 antigen ; CD4 antigen ; CD4-Positive T-Lymphocytes - immunology ; CD8 antigen ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - virology ; Cell cycle ; Cell growth ; CTLA-4 Antigen ; CTLA-4 protein ; Cytokines ; Cytotoxicity ; Foxp3 protein ; Growth factors ; HIV ; HIV-1 - immunology ; Human immunodeficiency virus ; Humans ; Immunoglobulins ; Immunology/Immune Response ; Immunology/Immunity to Infections ; Immunophenotyping ; Infections ; Infectious Diseases/HIV Infection and AIDS ; Interferon ; Interferon-gamma - biosynthesis ; Interleukin 10 ; Interleukin-10 - biosynthesis ; Lymphocytes ; Lymphocytes T ; Peptides ; Public health ; Receptors, Transforming Growth Factor beta ; Signal Transduction - immunology ; Signaling ; Species Specificity ; T cell receptors ; Transforming Growth Factor beta - biosynthesis ; γ-Interferon</subject><ispartof>PloS one, 2009-12, Vol.4 (12), p.e8194-e8194</ispartof><rights>2009 Elrefaei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Elrefaei et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-892efd5d6aad397acb6079dfad31af05988cd694c9e05a2b0233d97b534a81583</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791208/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791208/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20016783$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Elrefaei, Mohamed</creatorcontrib><creatorcontrib>Burke, Candace M</creatorcontrib><creatorcontrib>Baker, Chris A R</creatorcontrib><creatorcontrib>Jones, Norman G</creatorcontrib><creatorcontrib>Bousheri, Stephanie</creatorcontrib><creatorcontrib>Bangsberg, David R</creatorcontrib><creatorcontrib>Cao, Huyen</creatorcontrib><title>TGF-beta and IL-10 production by HIV-specific CD8+ T cells is regulated by CTLA-4 signaling on CD4+ T cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Immune dysregulation in HIV-1 infection is associated with increased expression of inhibitory molecules such as CTLA-4, TGF-beta, and IL-10. 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Our study suggests that CTLA-4 Signaling on CD4+ T cells regulates the inhibitory functions of the HIV-specific suppressor CD8+ T cells.</description><subject>Acquired immune deficiency syndrome</subject><subject>AIDS</subject><subject>Antigens</subject><subject>Antigens, CD - immunology</subject><subject>CD25 antigen</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8 antigen</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - virology</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>CTLA-4 Antigen</subject><subject>CTLA-4 protein</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Foxp3 protein</subject><subject>Growth factors</subject><subject>HIV</subject><subject>HIV-1 - immunology</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Immunology/Immune Response</subject><subject>Immunology/Immunity to Infections</subject><subject>Immunophenotyping</subject><subject>Infections</subject><subject>Infectious Diseases/HIV Infection and AIDS</subject><subject>Interferon</subject><subject>Interferon-gamma - 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In this study we examined one potential mechanism for regulating TGF-beta and IL-10 expression by HIV-specific suppressor CD8+ T cells. No overlap between TGF-beta, IL-10, and IFN-gamma cytokine production by HIV-specific CD8+ T cells was observed. TGF-beta positive and IL-10 positive cells were FOXP3 negative, CD25 negative, and displayed a heterogeneous surface expression of CD127. TGF-beta and IL-10 positive CD8+ T cells did not express CTLA-4. Nevertheless, CTLA-4 blockade resulted in a significant decrease in HIV-specific TGF-beta positive and IL-10 positive CD8+ T cell responses, and a concomitant increase in HIV-specific IFN-gamma positive CD8+ T cell responses. Depletion of CD4+ T cells abrogated the impact of CTLA-4 on HIV-specific TGF-beta positive and IL-10 positive CD8+ T cells. Our study suggests that CTLA-4 Signaling on CD4+ T cells regulates the inhibitory functions of the HIV-specific suppressor CD8+ T cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20016783</pmid><doi>10.1371/journal.pone.0008194</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Acquired immune deficiency syndrome AIDS Antigens Antigens, CD - immunology CD25 antigen CD4 antigen CD4-Positive T-Lymphocytes - immunology CD8 antigen CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - virology Cell cycle Cell growth CTLA-4 Antigen CTLA-4 protein Cytokines Cytotoxicity Foxp3 protein Growth factors HIV HIV-1 - immunology Human immunodeficiency virus Humans Immunoglobulins Immunology/Immune Response Immunology/Immunity to Infections Immunophenotyping Infections Infectious Diseases/HIV Infection and AIDS Interferon Interferon-gamma - biosynthesis Interleukin 10 Interleukin-10 - biosynthesis Lymphocytes Lymphocytes T Peptides Public health Receptors, Transforming Growth Factor beta Signal Transduction - immunology Signaling Species Specificity T cell receptors Transforming Growth Factor beta - biosynthesis γ-Interferon |
| title | TGF-beta and IL-10 production by HIV-specific CD8+ T cells is regulated by CTLA-4 signaling on CD4+ T cells |
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