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The role of \u03b3\u03b4 T cells is implicated in BD. The activation status of \u03b3\u03b4 T cells and their cytokine secretion against phosphoantigens are evaluated in BD.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>NKG2A, NKG2C, NKG2D, CD16 and CCR7 molecules on \u03b3\u03b4 T cells were analyzed in 70 BD, 27 tuberculosis (TB) patients and 26 healthy controls (HC). Peripheral \u03b3\u03b4 T cells were expanded with a phosphoantigen (BrHPP) and IL-2, restimulated with BrHPP and a TLR3 ligand, and cytokine production was measured.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>\u03b3\u03b4 T cells were not increased in both BD and TB patients, but the proportions of TCRV\u03b42<jats:sup>+<\/jats:sup> T cells were lower (58.9 and 50.7 vs. 71.7%, <jats:italic>P<\/jats:italic> = 0.04 and <jats:italic>P<\/jats:italic> = 0.005) compared to HC. Higher proportion of TCRV\u03b42<jats:sup>+<\/jats:sup> T cells were CD16<jats:sup>+<\/jats:sup> (26.2 and 33.9 vs. 16.6%, <jats:italic>P<\/jats:italic> = 0.02 and <jats:italic>P<\/jats:italic> = 0.001) and CCR7<jats:sup>-<\/jats:sup> (32.2 and 27.9 vs. 17.7%, <jats:italic>P<\/jats:italic> &lt; 0.0001 and <jats:italic>P<\/jats:italic> = 0.014) in BD and TB patients compared to HC. NKG2C<jats:sup>+<\/jats:sup> \u03b3\u03b4<jats:sup>+<\/jats:sup> T cells were relatively increased (0.5 and 0.6 vs. 0.3%, <jats:italic>P<\/jats:italic> = 0.008 and 0.018), whereas NKG2D positivity was decreased in patients with BD and TB (77.7 and 75.8 vs. 87.5%, <jats:italic>P<\/jats:italic> = 0.001 and 0.004). Expansion capacity of \u03b3\u03b4 T cells in BD and TB as well as production of IL-13, IFN-\u03b3, granulocyte monocyte colony stimulating factor (GM-CSF), TNF-\u03b1, CCL4 and CCL5 in BD was lower compared to HC, when restimulated by TLR3 ligand and BrHPP.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusion<\/jats:title>\n                        <jats:p>The changes on \u03b3\u03b4 T cells of BD as well as TB patients implicate that \u03b3\u03b4 T cells have already been exposed to regulatory effects, which changed their activity. Lower cytokine response of \u03b3\u03b4 T cells implicates down modulation of these cells in BD.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar4147","type":"journal-article","created":{"date-parts":[[2013,1,21]],"date-time":"2013-01-21T19:14:08Z","timestamp":1358795648000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Expression of regulatory receptors on \u03b3\u03b4 T Cells and their cytokine production in Behcet's disease"],"prefix":"10.1186","volume":"15","author":[{"given":"Gunes","family":"Parlakgul","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ekin","family":"Guney","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Burak","family":"Erer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zeki","family":"K\u0131l\u0131caslan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haner","family":"Direskeneli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ahmet","family":"Gul","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guher","family":"Saruhan-Direskeneli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2013,1,21]]},"reference":[{"key":"3881_CR1","doi-asserted-by":"publisher","first-page":"996","DOI":"10.1136\/ard.60.11.996","volume":"60","author":"H Direskeneli","year":"2001","unstructured":"Direskeneli H: Behcet's disease: infectious aetiology, new autoantigens, and HLA-B51. 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