{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T17:04:21Z","timestamp":1791651861091,"version":"4.3.4"},"reference-count":70,"publisher":"MDPI AG","issue":"24","license":[{"start":{"date-parts":[[2022,12,12]],"date-time":"2022-12-12T00:00:00Z","timestamp":1670803200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"China Medical University"},{"name":"Senior Jade Mountain Award"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Whereas autoimmune diseases are mediated primarily by T and B cells, auto-inflammatory syndromes (AIFS) involve natural killer cells, macrophages, mast cells, dendritic cells, different granulocyte subsets and complement components. In contrast to autoimmune diseases, the immune response of patients with AIFS is not associated with a breakdown of immune tolerance to self-antigens. Focusing on B lymphocyte subsets, this article offers a fresh perspective on the multiple cross-talks between both branches of innate and adaptive immunity in mounting coordinated signals that lead to AIFS. By virtue of their potential to play a role in adaptive immunity and to exert innate-like functions, B cells can be involved in both promoting inflammation and mitigating auto-inflammation in disorders that include mevalonate kinase deficiency syndrome, Kawasaki syndrome, inflammatory bone disorders, Schnitzler syndrome, Neuro-Beh\u00e7et\u2019s disease, and neuromyelitis optica spectrum disorder. Since there is a significant overlap between the pathogenic trajectories that culminate in autoimmune diseases, or AIFS, a more detailed understanding of their respective roles in the development of inflammation could lead to designing novel therapeutic avenues.<\/jats:p>","DOI":"10.3390\/cells11244025","type":"journal-article","created":{"date-parts":[[2022,12,13]],"date-time":"2022-12-13T02:59:01Z","timestamp":1670900341000},"page":"4025","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["B Cells at the Cross-Roads of Autoimmune Diseases and Auto-Inflammatory Syndromes"],"prefix":"10.3390","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8225-456X","authenticated-orcid":false,"given":"Moncef","family":"Zouali","sequence":"first","affiliation":[{"name":"Graduate Institute of Biomedical Sciences, China Medical University, Taichung City 404, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,12,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1016\/S0092-8674(00)80721-7","article-title":"Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes","volume":"97","author":"McDermott","year":"1999","journal-title":"Cell"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"102774","DOI":"10.1016\/j.autrev.2021.102774","article-title":"Systemic autoinflammatory disease in adults","volume":"20","author":"Betrains","year":"2021","journal-title":"Autoimmun. 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