Foxp3+ regulatory T cells among tuberculosis patients: impact on prognosis and restoration of antigen specific IFN-γ producing T cells
CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) and programmed death-1 (PD-1) molecules have emerged as pivotal players in immune suppression of chronic diseases. However, their impact on the disease severity, therapeutic response and restoration of immune response in human tuberculosis remains uncl...
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| Veröffentlicht in: | PloS one 2012-09, Vol.7 (9), p.e44728-e44728 |
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| creator | Singh, Amar Dey, Aparajita Ballave Mohan, Anant Sharma, Prabhat Kumar Mitra, Dipendra Kumar |
| description | CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) and programmed death-1 (PD-1) molecules have emerged as pivotal players in immune suppression of chronic diseases. However, their impact on the disease severity, therapeutic response and restoration of immune response in human tuberculosis remains unclear. Here, we describe the possible role of Treg cells, their M. tuberculosis driven expansion and contribution of PD-1 pathway to the suppressive function of Treg cells among pulmonary tuberculosis (PTB) patients. Multicolor flow cytometry, cell culture, cells sorting and ELISA were employed to execute the study. Our results showed significant increase in frequency of antigen-reactive Treg cells, which gradually declined during successful therapy and paralleled with decline of M. tuberculosis-specific IL-10 along with elevation of IFN-γ production, and raising the IFN-γ/IL-4 ratio. Interestingly, persistence of Treg cells tightly correlated with MDR tuberculosis. Also, we show that blocking PD-1/PD-L1 pathway abrogates Treg-mediated suppression, suggesting that the PD-1/PD-L1 pathway is required for Treg-mediated suppression of the antigen-specific T cells. Treg cells possibly play a role in dampening the effector immune response and abrogating PD-1 pathway on Treg cells significantly rescued protective T cell response, suggesting its importance in immune restoration among tuberculosis patients. |
| doi_str_mv | 10.1371/journal.pone.0044728 |
| format | Article |
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However, their impact on the disease severity, therapeutic response and restoration of immune response in human tuberculosis remains unclear. Here, we describe the possible role of Treg cells, their M. tuberculosis driven expansion and contribution of PD-1 pathway to the suppressive function of Treg cells among pulmonary tuberculosis (PTB) patients. Multicolor flow cytometry, cell culture, cells sorting and ELISA were employed to execute the study. Our results showed significant increase in frequency of antigen-reactive Treg cells, which gradually declined during successful therapy and paralleled with decline of M. tuberculosis-specific IL-10 along with elevation of IFN-γ production, and raising the IFN-γ/IL-4 ratio. Interestingly, persistence of Treg cells tightly correlated with MDR tuberculosis. Also, we show that blocking PD-1/PD-L1 pathway abrogates Treg-mediated suppression, suggesting that the PD-1/PD-L1 pathway is required for Treg-mediated suppression of the antigen-specific T cells. Treg cells possibly play a role in dampening the effector immune response and abrogating PD-1 pathway on Treg cells significantly rescued protective T cell response, suggesting its importance in immune restoration among tuberculosis patients.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0044728</identifier><identifier>PMID: 23028594</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Antigens ; Apoptosis ; Biology ; CD25 antigen ; CD4 antigen ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell culture ; Chronic illnesses ; Cytokines ; Cytometry ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Forkhead Transcription Factors - metabolism ; Foxp3 protein ; Gene expression ; Human behavior ; Humans ; Immune response ; Immune system ; Immunology ; Immunoregulation ; Infectious diseases ; Interferon ; Interferon-gamma - metabolism ; Interleukin 10 ; Interleukin 4 ; Interleukin-4 - metabolism ; Lymphocytes ; Lymphocytes T ; Male ; Medical prognosis ; Medicine ; Middle Aged ; Mycobacterium tuberculosis ; Patients ; PD-1 protein ; PD-L1 protein ; Programmed Cell Death 1 Receptor - metabolism ; Restoration ; T cell receptors ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; T-Lymphocytes, Regulatory - immunology ; T-Lymphocytes, Regulatory - metabolism ; Tropical diseases ; Tuberculosis ; Tuberculosis, Pulmonary - immunology ; Tuberculosis, Pulmonary - metabolism ; Tuberculosis, Pulmonary - pathology ; Viral infections ; Young Adult ; γ-Interferon</subject><ispartof>PloS one, 2012-09, Vol.7 (9), p.e44728-e44728</ispartof><rights>Singh 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 Singh et al 2012 Singh et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4418-acc6022f2efe4998068ecb00629f240bfab2bfa02633349f5ca2911347172b093</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/PMC3446959/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446959/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23028594$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Unutmaz, Derya</contributor><creatorcontrib>Singh, Amar</creatorcontrib><creatorcontrib>Dey, Aparajita Ballave</creatorcontrib><creatorcontrib>Mohan, Anant</creatorcontrib><creatorcontrib>Sharma, Prabhat Kumar</creatorcontrib><creatorcontrib>Mitra, Dipendra Kumar</creatorcontrib><title>Foxp3+ regulatory T cells among tuberculosis patients: impact on prognosis and restoration of antigen specific IFN-γ producing T cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) and programmed death-1 (PD-1) molecules have emerged as pivotal players in immune suppression of chronic diseases. However, their impact on the disease severity, therapeutic response and restoration of immune response in human tuberculosis remains unclear. Here, we describe the possible role of Treg cells, their M. tuberculosis driven expansion and contribution of PD-1 pathway to the suppressive function of Treg cells among pulmonary tuberculosis (PTB) patients. Multicolor flow cytometry, cell culture, cells sorting and ELISA were employed to execute the study. Our results showed significant increase in frequency of antigen-reactive Treg cells, which gradually declined during successful therapy and paralleled with decline of M. tuberculosis-specific IL-10 along with elevation of IFN-γ production, and raising the IFN-γ/IL-4 ratio. Interestingly, persistence of Treg cells tightly correlated with MDR tuberculosis. 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Treg cells possibly play a role in dampening the effector immune response and abrogating PD-1 pathway on Treg cells significantly rescued protective T cell response, suggesting its importance in immune restoration among tuberculosis patients.</description><subject>Adult</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Biology</subject><subject>CD25 antigen</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell culture</subject><subject>Chronic illnesses</subject><subject>Cytokines</subject><subject>Cytometry</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Foxp3 protein</subject><subject>Gene expression</subject><subject>Human behavior</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Immunoregulation</subject><subject>Infectious diseases</subject><subject>Interferon</subject><subject>Interferon-gamma - 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immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Cell culture</topic><topic>Chronic illnesses</topic><topic>Cytokines</topic><topic>Cytometry</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Foxp3 protein</topic><topic>Gene expression</topic><topic>Human behavior</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Immunoregulation</topic><topic>Infectious diseases</topic><topic>Interferon</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin 10</topic><topic>Interleukin 4</topic><topic>Interleukin-4 - metabolism</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Middle Aged</topic><topic>Mycobacterium tuberculosis</topic><topic>Patients</topic><topic>PD-1 protein</topic><topic>PD-L1 protein</topic><topic>Programmed Cell Death 1 Receptor - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Singh, Amar</au><au>Dey, Aparajita Ballave</au><au>Mohan, Anant</au><au>Sharma, Prabhat Kumar</au><au>Mitra, Dipendra Kumar</au><au>Unutmaz, Derya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Foxp3+ regulatory T cells among tuberculosis patients: impact on prognosis and restoration of antigen specific IFN-γ producing T cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-09-19</date><risdate>2012</risdate><volume>7</volume><issue>9</issue><spage>e44728</spage><epage>e44728</epage><pages>e44728-e44728</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) and programmed death-1 (PD-1) molecules have emerged as pivotal players in immune suppression of chronic diseases. However, their impact on the disease severity, therapeutic response and restoration of immune response in human tuberculosis remains unclear. Here, we describe the possible role of Treg cells, their M. tuberculosis driven expansion and contribution of PD-1 pathway to the suppressive function of Treg cells among pulmonary tuberculosis (PTB) patients. Multicolor flow cytometry, cell culture, cells sorting and ELISA were employed to execute the study. Our results showed significant increase in frequency of antigen-reactive Treg cells, which gradually declined during successful therapy and paralleled with decline of M. tuberculosis-specific IL-10 along with elevation of IFN-γ production, and raising the IFN-γ/IL-4 ratio. Interestingly, persistence of Treg cells tightly correlated with MDR tuberculosis. Also, we show that blocking PD-1/PD-L1 pathway abrogates Treg-mediated suppression, suggesting that the PD-1/PD-L1 pathway is required for Treg-mediated suppression of the antigen-specific T cells. Treg cells possibly play a role in dampening the effector immune response and abrogating PD-1 pathway on Treg cells significantly rescued protective T cell response, suggesting its importance in immune restoration among tuberculosis patients.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23028594</pmid><doi>10.1371/journal.pone.0044728</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Antigens Apoptosis Biology CD25 antigen CD4 antigen CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell culture Chronic illnesses Cytokines Cytometry Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Forkhead Transcription Factors - metabolism Foxp3 protein Gene expression Human behavior Humans Immune response Immune system Immunology Immunoregulation Infectious diseases Interferon Interferon-gamma - metabolism Interleukin 10 Interleukin 4 Interleukin-4 - metabolism Lymphocytes Lymphocytes T Male Medical prognosis Medicine Middle Aged Mycobacterium tuberculosis Patients PD-1 protein PD-L1 protein Programmed Cell Death 1 Receptor - metabolism Restoration T cell receptors T-Lymphocytes - immunology T-Lymphocytes - metabolism T-Lymphocytes, Regulatory - immunology T-Lymphocytes, Regulatory - metabolism Tropical diseases Tuberculosis Tuberculosis, Pulmonary - immunology Tuberculosis, Pulmonary - metabolism Tuberculosis, Pulmonary - pathology Viral infections Young Adult γ-Interferon |
| title | Foxp3+ regulatory T cells among tuberculosis patients: impact on prognosis and restoration of antigen specific IFN-γ producing T cells |
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