{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T14:17:38Z","timestamp":1778163458982,"version":"3.51.4"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,8,3]],"date-time":"2020-08-03T00:00:00Z","timestamp":1596412800000},"content-version":"vor","delay-in-days":215,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004410","name":"T\u00fcrkiye Bilimsel ve Teknolojik Ara\u015ft\u0131rma Kurumu","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004410","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Immunology Research"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:p>\n                    NLRP11 is a member of the PYD domain\u2010containing, nucleotide\u2010binding oligomerization\u2010domain (NOD\u2010) like receptor (NLR) family. The true stimulus of NLRP11 is still unclear to date, so the current study is built upon NLRP11 induction via adenosine stimulation and that activation can shape adaptive immune responses in a caspase\u20101\u2010independent manner. We examined the regulation and mechanism of adenosine responsiveness via NLRP11 in human Daudi Burkitt\u2019s B lymphoma cells and their effects on human peripheral CD4\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes from healthy individuals. NLRP11 was significantly upregulated after induction with adenosine at both the mRNA and protein levels, which led to the interaction of endogenous NLRP11 with the ASC adaptor protein; however, this interaction did not result in the activation of the caspase\u20101 enzyme. Furthermore, cocultures of NLRP11\u2010expressing Burkitt\u2019s lymphoma cells and na\u00efve human peripheral CD4\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes had reduced IFN\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    and IL\u201017A production, whereas IL\u201013 and IL\u201010 cytokines did not change. Interestingly, IFN\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    and IL\u201017A were recovered after transfection of Burkitt\u2019s lymphoma cells with siRNAs targeting NLRP11. Concomitant with NLRP11 upregulation, we also exhibited that adenosine A\n                    <jats:sub>2B<\/jats:sub>\n                    receptor signaling induced two phosphorylated downstream effectors, pErk1\/2 and pAkt (Ser473), but not pAkt (Thr308). Taken together, our data indicate that adenosine is a negative regulator of Th1 and Th17 responses via NLRP11 in an inflammasome\u2010independent manner.\n                  <\/jats:p>","DOI":"10.1155\/2020\/1421795","type":"journal-article","created":{"date-parts":[[2020,8,3]],"date-time":"2020-08-03T19:31:27Z","timestamp":1596483087000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Adenosine\u2010Induced NLRP11 in B Lymphoblasts Suppresses Human CD4\n                    <sup>+<\/sup>\n                    T Helper Cell 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