Differential expression of CD96 surface molecule represents CD8⁺ T cells with dissimilar effector function during HIV-1 infection
During HIV-1 infection, immune dysregulation and aberrant lymphocyte functions are well-established characteristics. Cell surface molecules are important for immunological functions and changes in expression can affect lymphocyte effector functions, thereby contributing to pathogenesis and disease p...
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description | During HIV-1 infection, immune dysregulation and aberrant lymphocyte functions are well-established characteristics. Cell surface molecules are important for immunological functions and changes in expression can affect lymphocyte effector functions, thereby contributing to pathogenesis and disease progression. In this study we have focused on CD96, a member of the IgG superfamily receptors that have generated increasing recent interest due to their adhesive and co-stimulatory functions in addition to immunoregulatory capacity. CD96 is expressed by both T and NK cells. Although the function of CD96 is not completely elucidated, it has been shown to have adhesive functions and enhance cytotoxicity. Interestingly, CD96 may also have inhibitory functions due to its immunoreceptor tyrosine-based inhibitory motif (ITIM). The clinical significance of CD96 is still comparatively limited although it has been associated with chronic Hepatitis B infection and disease progression. CD96 has not previously been studied in the context of HIV-1 infection, but due to its potential importance in immune regulation and relevance to chronic disease, we examined CD96 expression in relation to HIV-1 pathogenesis. In a cross-sectional analysis, we investigated the CD8(+) T cell expression of CD96 in cohorts of untreated HIV-1 infected adults with high viral loads (non-controllers) and low viral loads ("elite" controllers). We demonstrated that elite controllers have significantly higher CD96 mean fluorescence intensity on CD8(+) T cells compared to HIV-1 non-controllers and CD96 expression was positively associated with CD4(+) T cell counts. Functional assessment showed that CD8(+) T cells lacking CD96 expression represented a population that produced both perforin and IFN-γ following stimulation. Furthermore, CD96 expression on CD8(+) T cells was decreased in presence of lipopolysaccharide in vitro. Overall, these findings indicate that down-regulation of CD96 is an important aspect of HIV-1 pathogenesis and differential expression is related to cell effector functions and HIV-1 disease course. |
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Cell surface molecules are important for immunological functions and changes in expression can affect lymphocyte effector functions, thereby contributing to pathogenesis and disease progression. In this study we have focused on CD96, a member of the IgG superfamily receptors that have generated increasing recent interest due to their adhesive and co-stimulatory functions in addition to immunoregulatory capacity. CD96 is expressed by both T and NK cells. Although the function of CD96 is not completely elucidated, it has been shown to have adhesive functions and enhance cytotoxicity. Interestingly, CD96 may also have inhibitory functions due to its immunoreceptor tyrosine-based inhibitory motif (ITIM). The clinical significance of CD96 is still comparatively limited although it has been associated with chronic Hepatitis B infection and disease progression. CD96 has not previously been studied in the context of HIV-1 infection, but due to its potential importance in immune regulation and relevance to chronic disease, we examined CD96 expression in relation to HIV-1 pathogenesis. In a cross-sectional analysis, we investigated the CD8(+) T cell expression of CD96 in cohorts of untreated HIV-1 infected adults with high viral loads (non-controllers) and low viral loads ("elite" controllers). We demonstrated that elite controllers have significantly higher CD96 mean fluorescence intensity on CD8(+) T cells compared to HIV-1 non-controllers and CD96 expression was positively associated with CD4(+) T cell counts. Functional assessment showed that CD8(+) T cells lacking CD96 expression represented a population that produced both perforin and IFN-γ following stimulation. Furthermore, CD96 expression on CD8(+) T cells was decreased in presence of lipopolysaccharide in vitro. Overall, these findings indicate that down-regulation of CD96 is an important aspect of HIV-1 pathogenesis and differential expression is related to cell effector functions and HIV-1 disease course.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0051696</identifier><identifier>PMID: 23272144</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aberration ; Acquired immune deficiency syndrome ; Adults ; AIDS ; Antigens ; Antigens, CD - metabolism ; Biology ; Blood & organ donations ; CD4 antigen ; CD4 Lymphocyte Count ; CD8 antigen ; CD8-Positive T-Lymphocytes - cytology ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - metabolism ; Cell Differentiation - immunology ; Cell surface ; Chronic illnesses ; Chronic infection ; Cloning ; Control ; Controllers ; Cytotoxicity ; Disease Progression ; Down-Regulation ; Effector cells ; Fluorescence ; Gene Expression Regulation ; Hepatitis ; Hepatitis B ; HIV ; HIV Infections - immunology ; HIV Infections - metabolism ; HIV-1 - immunology ; Human immunodeficiency virus ; Humans ; Immunoglobulin G ; Immunology ; Immunoreceptor tyrosine-based inhibition motif ; Immunoregulation ; Infections ; Interferon ; Interferon-gamma - biosynthesis ; Leukocytes, Mononuclear - immunology ; Leukocytes, Mononuclear - metabolism ; Lipopolysaccharides ; Lipopolysaccharides - immunology ; Lymphocytes ; Lymphocytes T ; Medicine ; Pathogenesis ; Perforin ; Perforin - biosynthesis ; Receptors ; Studies ; T cell receptors ; Toxicity ; Tyrosine ; γ-Interferon</subject><ispartof>PloS one, 2012-12, Vol.7 (12), p.e51696</ispartof><rights>2012 Eriksson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (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>2012 Eriksson et al 2012 Eriksson et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-b64ac4a004bc82574ad4658eacd9b6e85da4ac9e5a588b82de5bfa23e04b5b263</citedby><cites>FETCH-LOGICAL-c526t-b64ac4a004bc82574ad4658eacd9b6e85da4ac9e5a588b82de5bfa23e04b5b263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521672/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521672/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2106,2932,23875,27933,27934,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23272144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lichterfeld, Mathias</contributor><creatorcontrib>Eriksson, Emily M</creatorcontrib><creatorcontrib>Keh, Chris E</creatorcontrib><creatorcontrib>Deeks, Steven G</creatorcontrib><creatorcontrib>Martin, Jeffrey N</creatorcontrib><creatorcontrib>Hecht, Frederick M</creatorcontrib><creatorcontrib>Nixon, Douglas F</creatorcontrib><title>Differential expression of CD96 surface molecule represents CD8⁺ T cells with dissimilar effector function during HIV-1 infection</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>During HIV-1 infection, immune dysregulation and aberrant lymphocyte functions are well-established characteristics. Cell surface molecules are important for immunological functions and changes in expression can affect lymphocyte effector functions, thereby contributing to pathogenesis and disease progression. In this study we have focused on CD96, a member of the IgG superfamily receptors that have generated increasing recent interest due to their adhesive and co-stimulatory functions in addition to immunoregulatory capacity. CD96 is expressed by both T and NK cells. Although the function of CD96 is not completely elucidated, it has been shown to have adhesive functions and enhance cytotoxicity. Interestingly, CD96 may also have inhibitory functions due to its immunoreceptor tyrosine-based inhibitory motif (ITIM). The clinical significance of CD96 is still comparatively limited although it has been associated with chronic Hepatitis B infection and disease progression. CD96 has not previously been studied in the context of HIV-1 infection, but due to its potential importance in immune regulation and relevance to chronic disease, we examined CD96 expression in relation to HIV-1 pathogenesis. In a cross-sectional analysis, we investigated the CD8(+) T cell expression of CD96 in cohorts of untreated HIV-1 infected adults with high viral loads (non-controllers) and low viral loads ("elite" controllers). We demonstrated that elite controllers have significantly higher CD96 mean fluorescence intensity on CD8(+) T cells compared to HIV-1 non-controllers and CD96 expression was positively associated with CD4(+) T cell counts. Functional assessment showed that CD8(+) T cells lacking CD96 expression represented a population that produced both perforin and IFN-γ following stimulation. Furthermore, CD96 expression on CD8(+) T cells was decreased in presence of lipopolysaccharide in vitro. Overall, these findings indicate that down-regulation of CD96 is an important aspect of HIV-1 pathogenesis and differential expression is related to cell effector functions and HIV-1 disease course.</description><subject>Aberration</subject><subject>Acquired immune deficiency syndrome</subject><subject>Adults</subject><subject>AIDS</subject><subject>Antigens</subject><subject>Antigens, CD - metabolism</subject><subject>Biology</subject><subject>Blood & organ donations</subject><subject>CD4 antigen</subject><subject>CD4 Lymphocyte Count</subject><subject>CD8 antigen</subject><subject>CD8-Positive T-Lymphocytes - cytology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cell Differentiation - immunology</subject><subject>Cell surface</subject><subject>Chronic illnesses</subject><subject>Chronic infection</subject><subject>Cloning</subject><subject>Control</subject><subject>Controllers</subject><subject>Cytotoxicity</subject><subject>Disease Progression</subject><subject>Down-Regulation</subject><subject>Effector cells</subject><subject>Fluorescence</subject><subject>Gene Expression Regulation</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>HIV</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - metabolism</subject><subject>HIV-1 - immunology</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Immunology</subject><subject>Immunoreceptor tyrosine-based inhibition motif</subject><subject>Immunoregulation</subject><subject>Infections</subject><subject>Interferon</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medicine</subject><subject>Pathogenesis</subject><subject>Perforin</subject><subject>Perforin - biosynthesis</subject><subject>Receptors</subject><subject>Studies</subject><subject>T cell receptors</subject><subject>Toxicity</subject><subject>Tyrosine</subject><subject>γ-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNp1ks1u1DAUhS0EoqXwBggssc4Q_ybZIKEp0JEqsSlsLce-nnrkiQc74WeJeCsehyfBYdKqXbCyde93zr26Ogg9J_WKsIa83sUpDTqsDnGAVV0LIjv5AJ2SjtFK0po9vPM_QU9y3hWItVI-RieU0YYSzk_Rr3PvHCQYRq8Dhu-HBDn7OODo8Pq8kzhPyWkDeB8DmCkATjAzRZAL0P75-RtfYQMhZPzNj9fY-qLf-6AThuJsxpiwmwYzzqZ2Sn7Y4ovN54pgP8ztUn6KHjkdMjxb3jP06f27q_VFdfnxw2b99rIygsqx6iXXhuu65r1pqWi4tlyKFrSxXS-hFVYXoAOhRdv2LbUgeqcpgyIQPZXsDL08-h5CzGq5X1akHIMwyTpWiM2RsFHv1CH5vU4_VNRe_SvEtFU6jd4EUE3XE1074MQy7gztOkGYA8ckNZQwW7zeLNOmfg_WlIslHe6Z3u8M_lpt41fFBCWyocXg1WKQ4pcJ8viflfmRMinmnMDdTiC1moNyo1JzUNQSlCJ7cXe7W9FNMthf9KW_kw</recordid><startdate>20121213</startdate><enddate>20121213</enddate><creator>Eriksson, Emily M</creator><creator>Keh, Chris E</creator><creator>Deeks, Steven G</creator><creator>Martin, Jeffrey N</creator><creator>Hecht, Frederick M</creator><creator>Nixon, Douglas F</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121213</creationdate><title>Differential expression of CD96 surface molecule represents CD8⁺ T cells with dissimilar effector function during HIV-1 infection</title><author>Eriksson, Emily M ; Keh, Chris E ; Deeks, Steven G ; Martin, Jeffrey N ; Hecht, Frederick M ; Nixon, Douglas F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-b64ac4a004bc82574ad4658eacd9b6e85da4ac9e5a588b82de5bfa23e04b5b263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aberration</topic><topic>Acquired immune deficiency syndrome</topic><topic>Adults</topic><topic>AIDS</topic><topic>Antigens</topic><topic>Antigens, CD - metabolism</topic><topic>Biology</topic><topic>Blood & organ donations</topic><topic>CD4 antigen</topic><topic>CD4 Lymphocyte Count</topic><topic>CD8 antigen</topic><topic>CD8-Positive T-Lymphocytes - cytology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - metabolism</topic><topic>Cell Differentiation - immunology</topic><topic>Cell surface</topic><topic>Chronic illnesses</topic><topic>Chronic infection</topic><topic>Cloning</topic><topic>Control</topic><topic>Controllers</topic><topic>Cytotoxicity</topic><topic>Disease Progression</topic><topic>Down-Regulation</topic><topic>Effector cells</topic><topic>Fluorescence</topic><topic>Gene Expression Regulation</topic><topic>Hepatitis</topic><topic>Hepatitis B</topic><topic>HIV</topic><topic>HIV Infections - immunology</topic><topic>HIV Infections - metabolism</topic><topic>HIV-1 - immunology</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Immunoglobulin G</topic><topic>Immunology</topic><topic>Immunoreceptor tyrosine-based inhibition motif</topic><topic>Immunoregulation</topic><topic>Infections</topic><topic>Interferon</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - immunology</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medicine</topic><topic>Pathogenesis</topic><topic>Perforin</topic><topic>Perforin - biosynthesis</topic><topic>Receptors</topic><topic>Studies</topic><topic>T cell receptors</topic><topic>Toxicity</topic><topic>Tyrosine</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eriksson, Emily M</creatorcontrib><creatorcontrib>Keh, Chris E</creatorcontrib><creatorcontrib>Deeks, Steven G</creatorcontrib><creatorcontrib>Martin, Jeffrey N</creatorcontrib><creatorcontrib>Hecht, Frederick M</creatorcontrib><creatorcontrib>Nixon, Douglas F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Cell surface molecules are important for immunological functions and changes in expression can affect lymphocyte effector functions, thereby contributing to pathogenesis and disease progression. In this study we have focused on CD96, a member of the IgG superfamily receptors that have generated increasing recent interest due to their adhesive and co-stimulatory functions in addition to immunoregulatory capacity. CD96 is expressed by both T and NK cells. Although the function of CD96 is not completely elucidated, it has been shown to have adhesive functions and enhance cytotoxicity. Interestingly, CD96 may also have inhibitory functions due to its immunoreceptor tyrosine-based inhibitory motif (ITIM). The clinical significance of CD96 is still comparatively limited although it has been associated with chronic Hepatitis B infection and disease progression. CD96 has not previously been studied in the context of HIV-1 infection, but due to its potential importance in immune regulation and relevance to chronic disease, we examined CD96 expression in relation to HIV-1 pathogenesis. In a cross-sectional analysis, we investigated the CD8(+) T cell expression of CD96 in cohorts of untreated HIV-1 infected adults with high viral loads (non-controllers) and low viral loads ("elite" controllers). We demonstrated that elite controllers have significantly higher CD96 mean fluorescence intensity on CD8(+) T cells compared to HIV-1 non-controllers and CD96 expression was positively associated with CD4(+) T cell counts. Functional assessment showed that CD8(+) T cells lacking CD96 expression represented a population that produced both perforin and IFN-γ following stimulation. Furthermore, CD96 expression on CD8(+) T cells was decreased in presence of lipopolysaccharide in vitro. Overall, these findings indicate that down-regulation of CD96 is an important aspect of HIV-1 pathogenesis and differential expression is related to cell effector functions and HIV-1 disease course.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23272144</pmid><doi>10.1371/journal.pone.0051696</doi><oa>free_for_read</oa></addata></record> |
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subjects | Aberration Acquired immune deficiency syndrome Adults AIDS Antigens Antigens, CD - metabolism Biology Blood & organ donations CD4 antigen CD4 Lymphocyte Count CD8 antigen CD8-Positive T-Lymphocytes - cytology CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - metabolism Cell Differentiation - immunology Cell surface Chronic illnesses Chronic infection Cloning Control Controllers Cytotoxicity Disease Progression Down-Regulation Effector cells Fluorescence Gene Expression Regulation Hepatitis Hepatitis B HIV HIV Infections - immunology HIV Infections - metabolism HIV-1 - immunology Human immunodeficiency virus Humans Immunoglobulin G Immunology Immunoreceptor tyrosine-based inhibition motif Immunoregulation Infections Interferon Interferon-gamma - biosynthesis Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Lipopolysaccharides Lipopolysaccharides - immunology Lymphocytes Lymphocytes T Medicine Pathogenesis Perforin Perforin - biosynthesis Receptors Studies T cell receptors Toxicity Tyrosine γ-Interferon |
title | Differential expression of CD96 surface molecule represents CD8⁺ T cells with dissimilar effector function during HIV-1 infection |
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