Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients
Summary Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects the arm and leg arteries of young smokers. The immune system seems to play a critical role in the aetiology of TAO; however, knowledge of the aspects involved in the progression of vascular tissue in...
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| creator | Dellalibera‐Joviliano, R. Joviliano, E. E. Silva, J. S. Evora, P. R. B. |
| description | Summary
Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects the arm and leg arteries of young smokers. The immune system seems to play a critical role in the aetiology of TAO; however, knowledge of the aspects involved in the progression of vascular tissue inflammation and, consequently, the evolution of this disease is still limited. This study was carried out to investigate the cytokine levels of tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐4, IL‐17 and IL‐23 in the plasma of TAO patients presenting with acute clinical manifestations. The study included 20 TAO patients (n = 10 women; n = 10 men) aged 38–59 years under clinical follow‐up, classified into two groups: (i) TAO former smokers (n = 11) and (ii) TAO active smokers (n = 9); the control groups included normal volunteer non‐smokers (n = 10, active smokers (n = 10) and former smokers (n = 10). Patients' plasma samples were measured using the sandwich enzyme‐linked immunosorbent assay. Statistical analyses were performed using the non‐parametric Mann–Whitney U‐test, with parameters significant at P |
| doi_str_mv | 10.1111/j.1365-2249.2012.04624.x |
| format | Article |
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Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects the arm and leg arteries of young smokers. The immune system seems to play a critical role in the aetiology of TAO; however, knowledge of the aspects involved in the progression of vascular tissue inflammation and, consequently, the evolution of this disease is still limited. This study was carried out to investigate the cytokine levels of tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐4, IL‐17 and IL‐23 in the plasma of TAO patients presenting with acute clinical manifestations. The study included 20 TAO patients (n = 10 women; n = 10 men) aged 38–59 years under clinical follow‐up, classified into two groups: (i) TAO former smokers (n = 11) and (ii) TAO active smokers (n = 9); the control groups included normal volunteer non‐smokers (n = 10, active smokers (n = 10) and former smokers (n = 10). Patients' plasma samples were measured using the sandwich enzyme‐linked immunosorbent assay. Statistical analyses were performed using the non‐parametric Mann–Whitney U‐test, with parameters significant at P < 0·05. The activities of all cytokines were different in groups of TAO patients when compared with normal controls, and decreased for control smokers. Increased levels of TNF‐α, IL‐1β, IL‐4, IL‐17 and IL‐23 were significant in patients with TAO when compared to the controls (P < 0·005, all parameters). The results presented here indicate an increased production of cytokines in TAO, possibly contributing to the inflammatory response observed in the patients' vascular levels. In addition, the increased levels of IL‐17 and IL‐23 suggest that the disturbance of TAO is involved with mechanisms of autoimmunity. Thus, the discovery of IL‐17 and its association with inflammation and autoimmune pathology has reshaped our viewpoint regarding the pathogenesis of TAO, which was based previously on the T helper type 1 (Th1)–Th2 paradigm.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.2012.04624.x</identifier><identifier>PMID: 22943198</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Analytical, structural and metabolic biochemistry ; Arm ; Arteries ; autoimmune disease ; Autoimmunity ; Autoimmunity - immunology ; Biological and medical sciences ; Buerger's disease ; Case-Control Studies ; Cytokines ; Cytokines - blood ; Cytokines - immunology ; Enzyme-Linked Immunosorbent Assay ; Evolution ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Immune system ; Inflammation ; Inflammation - blood ; Inflammation - immunology ; Inflammatory diseases ; Interleukin 1 ; Interleukin 17 ; Interleukin 23 ; Interleukin 4 ; Interleukin-1 - blood ; Interleukin-1 - immunology ; Interleukin-17 - blood ; Interleukin-17 - immunology ; Interleukin-23 - blood ; Interleukin-23 - immunology ; Interleukin-4 - blood ; Interleukin-4 - immunology ; Leg ; Male ; Medical sciences ; Middle Aged ; Original ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Smoking - blood ; Smoking - immunology ; Statistical analysis ; Statistics, Nonparametric ; T-Lymphocytes, Helper-Inducer - immunology ; thromboangiitis obliterans ; Thromboangiitis Obliterans - blood ; Thromboangiitis Obliterans - immunology ; Tumor necrosis factor- alpha ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>Clinical and experimental immunology, 2012-10, Vol.170 (1), p.28-35</ispartof><rights>2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology</rights><rights>2015 INIST-CNRS</rights><rights>2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology.</rights><rights>2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5654-39fb3dcfd51f25394f294fa7146f1be6e77e357dd874402e4ea80a83268e33643</citedby><cites>FETCH-LOGICAL-c5654-39fb3dcfd51f25394f294fa7146f1be6e77e357dd874402e4ea80a83268e33643</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/PMC3444714/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444714/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26351971$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22943198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dellalibera‐Joviliano, R.</creatorcontrib><creatorcontrib>Joviliano, E. E.</creatorcontrib><creatorcontrib>Silva, J. S.</creatorcontrib><creatorcontrib>Evora, P. R. B.</creatorcontrib><title>Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects the arm and leg arteries of young smokers. The immune system seems to play a critical role in the aetiology of TAO; however, knowledge of the aspects involved in the progression of vascular tissue inflammation and, consequently, the evolution of this disease is still limited. This study was carried out to investigate the cytokine levels of tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐4, IL‐17 and IL‐23 in the plasma of TAO patients presenting with acute clinical manifestations. The study included 20 TAO patients (n = 10 women; n = 10 men) aged 38–59 years under clinical follow‐up, classified into two groups: (i) TAO former smokers (n = 11) and (ii) TAO active smokers (n = 9); the control groups included normal volunteer non‐smokers (n = 10, active smokers (n = 10) and former smokers (n = 10). Patients' plasma samples were measured using the sandwich enzyme‐linked immunosorbent assay. Statistical analyses were performed using the non‐parametric Mann–Whitney U‐test, with parameters significant at P < 0·05. The activities of all cytokines were different in groups of TAO patients when compared with normal controls, and decreased for control smokers. Increased levels of TNF‐α, IL‐1β, IL‐4, IL‐17 and IL‐23 were significant in patients with TAO when compared to the controls (P < 0·005, all parameters). The results presented here indicate an increased production of cytokines in TAO, possibly contributing to the inflammatory response observed in the patients' vascular levels. In addition, the increased levels of IL‐17 and IL‐23 suggest that the disturbance of TAO is involved with mechanisms of autoimmunity. Thus, the discovery of IL‐17 and its association with inflammation and autoimmune pathology has reshaped our viewpoint regarding the pathogenesis of TAO, which was based previously on the T helper type 1 (Th1)–Th2 paradigm.</description><subject>Adult</subject><subject>Analytical, structural and metabolic biochemistry</subject><subject>Arm</subject><subject>Arteries</subject><subject>autoimmune disease</subject><subject>Autoimmunity</subject><subject>Autoimmunity - immunology</subject><subject>Biological and medical sciences</subject><subject>Buerger's disease</subject><subject>Case-Control Studies</subject><subject>Cytokines</subject><subject>Cytokines - blood</subject><subject>Cytokines - immunology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Evolution</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - immunology</subject><subject>Inflammatory diseases</subject><subject>Interleukin 1</subject><subject>Interleukin 17</subject><subject>Interleukin 23</subject><subject>Interleukin 4</subject><subject>Interleukin-1 - blood</subject><subject>Interleukin-1 - immunology</subject><subject>Interleukin-17 - blood</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-23 - blood</subject><subject>Interleukin-23 - immunology</subject><subject>Interleukin-4 - blood</subject><subject>Interleukin-4 - immunology</subject><subject>Leg</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Smoking - blood</subject><subject>Smoking - immunology</subject><subject>Statistical analysis</subject><subject>Statistics, Nonparametric</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>thromboangiitis obliterans</subject><subject>Thromboangiitis Obliterans - blood</subject><subject>Thromboangiitis Obliterans - immunology</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk1vEzEQhi0EoqHwF9BKCInLBn_v-gBSFbVQqRIXOFter9047NrB9qaNxI-vl4TwcaovtjXPvDP2OwBUCC5RWe83S0Q4qzGmYokhwktIOabL-ydgcQo8BQsIoagFgvQMvEhpU66cc_wcnGEsKEGiXYCfFzq7ncou-CrYSu9z-O68SZUOMYYuRJVNdefyuurNzgxhOxqfZ9J5O6hxPGQq31dqysGN4-Rd3pdoldcxjF1Q_ta57FIVusFlE5VP1bZkFZn0Ejyzakjm1XE_B9-uLr-uPtc3Xz5dry5uas04ozURtiO9tj1DFjMiqC3tW9Ugyi3qDDdNYwhr-r5tKIXYUKNaqFqCeWsI4ZScg48H3e3UjabXpXZUg9xGN6q4l0E5-W_Eu7W8DTtJKKWlTBF4dxSI4cdkUpajS9oMg_ImTEkiyEXxgTXwEShpYYMEQgV98x-6CVP05SckYpS1nJOWFKo9UDqGlKKxp74RlPM0yI2cTZez6XKeBvlrGuR9SX3997tPib_tL8DbI6CSVoMt7miX_nCcMCSaudMPB-7ODWb_6Abk6vJ6PpEHhtLTOg</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Dellalibera‐Joviliano, R.</creator><creator>Joviliano, E. E.</creator><creator>Silva, J. S.</creator><creator>Evora, P. R. B.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Oxford University Press</general><general>Blackwell Science Inc</general><scope>IQODW</scope><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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201210</creationdate><title>Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients</title><author>Dellalibera‐Joviliano, R. ; Joviliano, E. E. ; Silva, J. S. ; Evora, P. R. B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5654-39fb3dcfd51f25394f294fa7146f1be6e77e357dd874402e4ea80a83268e33643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Analytical, structural and metabolic biochemistry</topic><topic>Arm</topic><topic>Arteries</topic><topic>autoimmune disease</topic><topic>Autoimmunity</topic><topic>Autoimmunity - immunology</topic><topic>Biological and medical sciences</topic><topic>Buerger's disease</topic><topic>Case-Control Studies</topic><topic>Cytokines</topic><topic>Cytokines - blood</topic><topic>Cytokines - immunology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Evolution</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - immunology</topic><topic>Inflammatory diseases</topic><topic>Interleukin 1</topic><topic>Interleukin 17</topic><topic>Interleukin 23</topic><topic>Interleukin 4</topic><topic>Interleukin-1 - blood</topic><topic>Interleukin-1 - immunology</topic><topic>Interleukin-17 - blood</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-23 - blood</topic><topic>Interleukin-23 - immunology</topic><topic>Interleukin-4 - blood</topic><topic>Interleukin-4 - immunology</topic><topic>Leg</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Smoking - blood</topic><topic>Smoking - immunology</topic><topic>Statistical analysis</topic><topic>Statistics, Nonparametric</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>thromboangiitis obliterans</topic><topic>Thromboangiitis Obliterans - blood</topic><topic>Thromboangiitis Obliterans - immunology</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dellalibera‐Joviliano, R.</creatorcontrib><creatorcontrib>Joviliano, E. E.</creatorcontrib><creatorcontrib>Silva, J. S.</creatorcontrib><creatorcontrib>Evora, P. R. B.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dellalibera‐Joviliano, R.</au><au>Joviliano, E. E.</au><au>Silva, J. S.</au><au>Evora, P. R. B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2012-10</date><risdate>2012</risdate><volume>170</volume><issue>1</issue><spage>28</spage><epage>35</epage><pages>28-35</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Summary
Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects the arm and leg arteries of young smokers. The immune system seems to play a critical role in the aetiology of TAO; however, knowledge of the aspects involved in the progression of vascular tissue inflammation and, consequently, the evolution of this disease is still limited. This study was carried out to investigate the cytokine levels of tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐4, IL‐17 and IL‐23 in the plasma of TAO patients presenting with acute clinical manifestations. The study included 20 TAO patients (n = 10 women; n = 10 men) aged 38–59 years under clinical follow‐up, classified into two groups: (i) TAO former smokers (n = 11) and (ii) TAO active smokers (n = 9); the control groups included normal volunteer non‐smokers (n = 10, active smokers (n = 10) and former smokers (n = 10). Patients' plasma samples were measured using the sandwich enzyme‐linked immunosorbent assay. Statistical analyses were performed using the non‐parametric Mann–Whitney U‐test, with parameters significant at P < 0·05. The activities of all cytokines were different in groups of TAO patients when compared with normal controls, and decreased for control smokers. Increased levels of TNF‐α, IL‐1β, IL‐4, IL‐17 and IL‐23 were significant in patients with TAO when compared to the controls (P < 0·005, all parameters). The results presented here indicate an increased production of cytokines in TAO, possibly contributing to the inflammatory response observed in the patients' vascular levels. In addition, the increased levels of IL‐17 and IL‐23 suggest that the disturbance of TAO is involved with mechanisms of autoimmunity. Thus, the discovery of IL‐17 and its association with inflammation and autoimmune pathology has reshaped our viewpoint regarding the pathogenesis of TAO, which was based previously on the T helper type 1 (Th1)–Th2 paradigm.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22943198</pmid><doi>10.1111/j.1365-2249.2012.04624.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Adult Analytical, structural and metabolic biochemistry Arm Arteries autoimmune disease Autoimmunity Autoimmunity - immunology Biological and medical sciences Buerger's disease Case-Control Studies Cytokines Cytokines - blood Cytokines - immunology Enzyme-Linked Immunosorbent Assay Evolution Female Fundamental and applied biological sciences. Psychology Humans Immune system Inflammation Inflammation - blood Inflammation - immunology Inflammatory diseases Interleukin 1 Interleukin 17 Interleukin 23 Interleukin 4 Interleukin-1 - blood Interleukin-1 - immunology Interleukin-17 - blood Interleukin-17 - immunology Interleukin-23 - blood Interleukin-23 - immunology Interleukin-4 - blood Interleukin-4 - immunology Leg Male Medical sciences Middle Aged Original Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Smoking - blood Smoking - immunology Statistical analysis Statistics, Nonparametric T-Lymphocytes, Helper-Inducer - immunology thromboangiitis obliterans Thromboangiitis Obliterans - blood Thromboangiitis Obliterans - immunology Tumor necrosis factor- alpha Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - immunology |
| title | Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients |
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