{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T07:15:31Z","timestamp":1789802131979,"version":"4.0.1"},"reference-count":76,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2023,2,8]],"date-time":"2023-02-08T00:00:00Z","timestamp":1675814400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,2,8]],"date-time":"2023-02-08T00:00:00Z","timestamp":1675814400000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,2,8]],"date-time":"2023-02-08T00:00:00Z","timestamp":1675814400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["LA 1262\/8-1"],"award-info":[{"award-number":["LA 1262\/8-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["CDC 1181_A02"],"award-info":[{"award-number":["CDC 1181_A02"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["CO 1469\/16-1"],"award-info":[{"award-number":["CO 1469\/16-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2023,1,30]]},"abstract":"<jats:p>\n                    The myeloid C-type lectin receptor (CLR) MINCLE senses the mycobacterial cell wall component trehalose-6,6\u2019-dimycolate (TDM). Recently, we found that IL-4 downregulates MINCLE expression in macrophages. IL-4 is a hallmark cytokine in helminth infections, which appear to increase the risk for mycobacterial infection and active tuberculosis. Here, we investigated functional consequences of IL-4 and helminth infection on MINCLE-driven macrophage activation and Th1\/Th17 adjuvanticity. IL-4 inhibited MINCLE and cytokine induction after macrophage infection with\n                    <jats:italic>Mycobacterium bovis<\/jats:italic>\n                    bacille Calmette-Guerin (BCG). Infection of mice with BCG upregulated MINCLE on myeloid cells, which was inhibited by IL-4 plasmid injection and by infection with the nematode\n                    <jats:italic>Nippostrongylus brasiliensis<\/jats:italic>\n                    in monocytes. To determine the impact of helminth infection on MINCLE-dependent immune responses, we vaccinated mice with a recombinant protein together with the MINCLE ligand trehalose-6,6-dibehenate (TDB) as adjuvant. Concurrent infection with\n                    <jats:italic>N. brasiliensis<\/jats:italic>\n                    or with\n                    <jats:italic>Schistosoma mansoni<\/jats:italic>\n                    promoted T cell-derived IL-4 production and suppressed Th1\/Th17 differentiation in the spleen. In contrast, helminth infection did not reduce Th1\/Th17 induction by TDB in draining peripheral lymph nodes, where IL-4 levels were unaltered. Upon use of the TLR4-dependent adjuvant G3D6A,\n                    <jats:italic>N. brasiliensis<\/jats:italic>\n                    infection impaired selectively the induction of splenic antigen-specific Th1 but not of Th17 cells. Inhibition of MINCLE-dependent Th1\/Th17 responses in mice infected with\n                    <jats:italic>N. brasiliensis<\/jats:italic>\n                    was dependent on IL-4\/IL-13. Thus, helminth infection attenuated the Th17 response to MINCLE-dependent immunization in an organ- and adjuvant-specific manner via the Th2 cytokines IL-4\/IL-13. Taken together, our results demonstrate downregulation of MINCLE expression on monocytes and macrophages by IL-4 as a possible mechanism of thwarted Th17 vaccination responses by underlying helminth infection.\n                  <\/jats:p>","DOI":"10.7554\/elife.72923","type":"journal-article","created":{"date-parts":[[2023,1,30]],"date-time":"2023-01-30T05:18:33Z","timestamp":1675055913000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.72923","source":"Crossref","is-referenced-by-count":21,"title":["IL-4 and helminth infection downregulate MINCLE-dependent macrophage response to mycobacteria and Th17 adjuvanticity"],"prefix":"10.7554","volume":"12","author":[{"given":"Judith","family":"Schick","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0030f2a11","id-type":"ROR","asserted-by":"publisher"}],"name":"Institut f\u00fcr Klinische Mikrobiologie, Immunologie und Hygiene, Universit\u00e4tsklinikum Erlangen, Friedrich-Alexander Universit\u00e4t 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