{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T01:14:21Z","timestamp":1777943661325,"version":"3.51.4"},"reference-count":44,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2020,2,16]],"date-time":"2020-02-16T00:00:00Z","timestamp":1581811200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Vascular"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Atherosclerosis is considered as a chronic inflammatory disorder where the central role of T cells in its pathogenesis is well known. T helper-9 cells have a distinctive effect upon the inflammatory processes. They stimulate macrophages via secretion of their cytokine interleukin-9. Based on its known involvement with other inflammatory disorders, we hypothesized that interleukin-9 might be associated with the inflammatory limb of peripheral atherosclerotic disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We tested this hypothesis on peripheral blood mononuclear cells (PBMCs) and freshly resected arterial tissues from 84 patients with peripheral arterial occlusive disease (PAOD) and 50 non-atherosclerotic subjects. A number of experimental methods were used including flow cytometry analysis of T helper-9 cells using anti-CD3, anti-CD4, and anti-interleukin-9monoclonal antibodies as well as real-time polymerase chain reaction for the assessment of gene expression of interleukin-9. In addition, circulating serum levels of interleukin-9 were measured using enzyme linked immunosorbent assay. We also evaluated the ability of recombinant interleukin-9 to modulate IL-17 release in cultured isolated CD3+ T cells with relation to atherosclerotic disorder in vitro.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and conclusions<\/jats:title>\n                    <jats:p>Here we report increased percentages of T helper-9 cells and interleukin-9 levels in patients with chronic lower limb atherosclerotic ischemia, compared to healthy controls. Through investigation of different atherosclerotic patient populations with different disease stages, we found elevated interleukin-9 level both systemically and within the lesion and increased expression of cells in severe disease stages. The current study also revealed enhanced expression of mRNA levels of interleukin-9 within the atherosclerotic lesion when compared with non-atherosclerotic vessels. Levels of released IL-17 in CD3+ T cell culture supernatants supplemented with interleukin-9 were significantly positively correlated in the enrolled patients. The results suggest a role for T helper-9 cells and IL-9 in atherosclerotic process, potentially involving IL-17-mediated mechanisms. Indeed, we found that interleukin-9 promoted IL-17 release in PBMCs, with a particularly marked response in severe disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1708538120905430","type":"journal-article","created":{"date-parts":[[2020,2,17]],"date-time":"2020-02-17T00:35:52Z","timestamp":1581899752000},"page":"378-389","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Changes and significance of T helper-9 cells and interleukin-9 in patients with atherosclerotic chronic lower limb ischemia: Effect on IL-17 release"],"prefix":"10.1177","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5854-7736","authenticated-orcid":false,"given":"Mai","family":"Moaaz","sequence":"first","affiliation":[{"name":"Department of Immunology and Allergy, Medical Research Institute, Alexandria University, Alexandria, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hassan","family":"Lotfy","sequence":"additional","affiliation":[{"name":"Department of Surgery, Vascular Surgery Unit, Faculty of Medicine, Alexandria University, Alexandria, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2020,2,16]]},"reference":[{"key":"bibr1-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(13)61249-0"},{"key":"bibr2-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1007\/s00772-018-0380-1"},{"key":"bibr3-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1161\/hc0902.104353"},{"key":"bibr4-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1038\/nri1882"},{"key":"bibr5-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2011.02.012"},{"key":"bibr6-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2009.07.152"},{"key":"bibr7-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.111.261784"},{"key":"bibr8-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20090545"},{"key":"bibr9-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.111.229997"},{"key":"bibr10-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1867"},{"key":"bibr11-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-6877-0_2"},{"key":"bibr12-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1038\/nri2848"},{"key":"bibr13-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0812530106"},{"key":"bibr14-1708538120905430","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20090246"},{"key":"bibr15-1708538120905430","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1003307"},{"key":"bibr16-1708538120905430","first-page":"CD010680","volume":"9","author":"Welch 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