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Despite the complexity and effectiveness of the immune response, the parasite has developed many strategies to evade it and take control of the host cell to replicate. These evasion strategies start at early stages of infection by hijacking immune receptors to mitigate the cellular response. In this study, we examined whether\n                      <jats:italic>Leishmania<\/jats:italic>\n                      uses the Fc receptor Fc\u03b3RIIA\/CD32a and its downstream signaling pathways to evade the host immune response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Regarding in vivo studies, CD32a transgenic mice and the corresponding wild types were infected with\n                      <jats:italic>Leishmania major<\/jats:italic>\n                      Friedlin strain. For the in vitro experiments, BMDMs isolated from WT or CD32a transgenic mice and control or CD32a knockdown differentiated THP-1s were infected with two species of\n                      <jats:italic>Leishmania<\/jats:italic>\n                      ,\n                      <jats:italic>Leishmania major<\/jats:italic>\n                      and\n                      <jats:italic>L. tropica.<\/jats:italic>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In vivo, expression of Fc\u03b3RIIA\/CD32a was found to accelerate the signs of inflammation while simultaneously preventing the formation of necrotic lesions after\n                      <jats:italic>Leishmania<\/jats:italic>\n                      infection. In infected macrophages, the presence of Fc\u03b3RIIA\/CD32a did not affect the secretion of proinflammatory cytokines, while the balance between ITAMa and ITAMi proteins was disturbed with improved Fyn and Lyn activation. Unexpectedly, infection with\n                      <jats:italic>L. tropica<\/jats:italic>\n                      but not\n                      <jats:italic>L. major<\/jats:italic>\n                      triggered an intracytoplasmic processing of Fc\u03b3RIIA\/CD32a.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our observations underscore the significance of Fc\u03b3RIIA\/CD32a in cutaneous leishmaniasis and its potential use as a therapeutic target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1186\/s13071-024-06593-y","type":"journal-article","created":{"date-parts":[[2024,12,18]],"date-time":"2024-12-18T13:09:52Z","timestamp":1734527392000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["FcR\u03b3IIA attenuates pathology of cutaneous leishmaniasis and modulates ITAMa\/i balance"],"prefix":"10.1186","volume":"17","author":[{"given":"Ikram","family":"Hammi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julien","family":"Giron-Michel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myriam","family":"Riyad","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Khadija","family":"Akarid","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Damien","family":"Arnoult","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,12,18]]},"reference":[{"key":"6593_CR1","unstructured":"WHO World Health Organization; 2024. https:\/\/apps.who.int\/neglected_diseases\/ntddata\/leishmaniasis\/leishmaniasis.html."},{"key":"6593_CR2","doi-asserted-by":"publisher","first-page":"232","DOI":"10.1016\/j.annder.2019.02.002","volume":"146","author":"M Mokni","year":"2019","unstructured":"Mokni M. 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