{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:16:10Z","timestamp":1787026570817,"version":"build-2736575974"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,12,10]],"date-time":"2021-12-10T00:00:00Z","timestamp":1639094400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000038","name":"Natural Sciences and Engineering Research Council of Canada","doi-asserted-by":"publisher","award":["RGPIN-2016-04349"],"award-info":[{"award-number":["RGPIN-2016-04349"]}],"id":[{"id":"10.13039\/501100000038","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Interleukin-15, produced by hematopoietic and parenchymal cells, maintains immune cell homeostasis and facilitates activation of lymphoid and myeloid cell subsets. IL-15 interacts with the ligand-binding receptor chain IL-15R\u03b1 during biosynthesis, and the IL-15:IL-15R\u03b1 complex is trans-presented to responder cells that express the IL-2\/15R\u03b2\u03b3\n                    <jats:sub>c<\/jats:sub>\n                    complex to initiate signaling. IL-15-deficient and IL-15R\u03b1-deficient mice display similar alterations in immune cell subsets. Thus, the trimeric IL-15R\u03b1\u03b2\u03b3\n                    <jats:sub>c<\/jats:sub>\n                    complex is considered the functional IL-15 receptor. However, studies on the pathogenic role of IL-15 in inflammatory and autoimmune diseases indicate that IL-15 can signal independently of IL-15R\u03b1\n                    <jats:italic>via<\/jats:italic>\n                    the IL-15R\u03b2\u03b3\n                    <jats:sub>c<\/jats:sub>\n                    dimer. Here, we compared the ability of mice lacking IL-15 (no signaling) or IL-15R\u03b1 (partial\/distinct signaling) to control\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    infection. We show that IL-15-deficient mice succumb to infection whereas IL-15R\u03b1-deficient mice clear the pathogen as efficiently as wildtype mice. IL-15-deficient macrophages did not show any defect in bacterial uptake or iNOS expression\n                    <jats:italic>in vitro<\/jats:italic>\n                    .\n                    <jats:italic>In vivo<\/jats:italic>\n                    , IL-15 deficiency impaired the accumulation of inflammatory monocytes in infected spleens without affecting chemokine and pro-inflammatory cytokine production. The inability of IL-15-deficient mice to clear\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    results from impaired early IFN\u03b3 production, which was not affected in IL-15R\u03b1-deficient mice. Administration of IFN\u03b3 partially enabled IL-15-deficient mice to control the infection. Bone marrow chimeras revealed that IL-15 needed for early bacterial control can originate from both hematopoietic and non-hematopoietic cells. Overall, our findings indicate that IL-15-dependent IL-15R\u03b1-independent signaling\n                    <jats:italic>via<\/jats:italic>\n                    the IL-15R\u03b2\u03b3\n                    <jats:sub>c<\/jats:sub>\n                    dimeric complex is necessary and sufficient for the induction of IFN\u03b3 from sources other than NK\/NKT cells to control bacterial pathogens.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2021.793918","type":"journal-article","created":{"date-parts":[[2021,12,10]],"date-time":"2021-12-10T04:16:05Z","timestamp":1639109765000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["IL-15R\u03b1-Independent IL-15 Signaling in Non-NK Cell-Derived IFN\u03b3 Driven Control of Listeria monocytogenes"],"prefix":"10.3389","volume":"12","author":[{"given":"Madhuparna","family":"Nandi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitterrand Muamba","family":"Moyo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sakina","family":"Orkhis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeanne Masunga Faida","family":"Mobulakani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc-Andr\u00e9","family":"Limoges","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fjolla","family":"Rexhepi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marian","family":"Mayhue","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anny Armas","family":"Cayarga","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gisela Cofino","family":"Marrero","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Subburaj","family":"Ilangumaran","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alfredo","family":"Menendez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheela","family":"Ramanathan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,12,10]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80246-0","article-title":"IL-15: A Pleiotropic Cytokine With Diverse Receptor\/Signaling Pathways Whose Expression Is Controlled at Multiple 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