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This hypothesis suggests that in a subset of patients, immune dysregulation, especially involving interleukins (ILs), contributes to depression. This review compares IL dysregulation in MDD and autoimmune diseases to identify common and unique inflammatory mechanisms for treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and Conclusion<\/jats:title>\n                    <jats:p>Some MDD patients exhibit chronic, low\u2010grade inflammation both systemically (in blood) and centrally (in CSF and brain). They show elevated pro\u2010inflammatory IL\u20106, IL\u20101\u03b2, and IL\u201018, with insufficient anti\u2010inflammatory IL\u201010. This immune dysregulation affects key neurobiological processes (monoamine metabolism, HPA axis, neurogenesis), linking inflammation to depressive symptoms. MDD and autoimmune diseases share inflammatory mediators and signaling pathways, supporting these as therapeutic targets; however, MDD's inflammation is low\u2010grade and innate driven, whereas autoimmune diseases have high\u2010grade, adaptive immune responses to specific antigens. Successful anti\u2010IL therapies in autoimmune conditions provide a roadmap for treating inflammation\u2010driven depression. Translating these findings to practice requires a precision immune\u2010psychiatry approach. Biomarkers like C\u2010reactive protein and IL\u20106 can identify an inflammatory depression subtype, and patients may benefit from targeted immunomodulatory strategies, repurposed biologics, novel small molecules, or lifestyle interventions particularly if standard antidepressants fail.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70791","type":"journal-article","created":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T08:58:31Z","timestamp":1771318711000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Interleukins in Major Depressive Disorder: Lessons From Autoimmune Diseases and Pathways to Clinical Translation"],"prefix":"10.1002","volume":"32","author":[{"given":"Adnan","family":"Akif","sequence":"first","affiliation":[{"name":"Department of Physiology &amp; Cell Biology, School of Medicine University of Nevada  Reno Nevada USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad Fahim","family":"Kadir","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Campbell University School of Osteopathic Medicine  Buies Creek North Carolina USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2820-3144","authenticated-orcid":false,"given":"Md. Rabiul","family":"Islam","sequence":"additional","affiliation":[{"name":"School of Pharmacy BRAC University  Dhaka Bangladesh"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,2,17]]},"reference":[{"key":"e_1_2_11_2_1","unstructured":"WHO. 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