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At a high level, initial allergen exposure disrupts epithelial integrity, triggering local inflammation via alarmins including IL\u201025, IL\u201033, and TSLP, which activate type 2 innate lymphoid cells as well as other immune cells to secrete type 2 cytokines IL\u20104, IL\u20105 and IL\u201013, promoting Th2 cell development and eosinophil recruitment. Th2 cell dependent B cell activation promotes the production of allergen\u2010specific IgE, which stably binds to basophils and mast cells. Rapid degranulation of these cells upon allergen re\u2010exposure leads to allergic symptoms. Recent advances in our understanding of the molecular and cellular mechanisms underlying allergic pathophysiology have significantly shaped the development of therapeutic intervention strategies. In this review, we highlight key therapeutic targets within the allergic cascade with a particular focus on past, current and future treatment approaches using monoclonal antibodies. Specific targeting of alarmins, type 2 cytokines and IgE has shown varying degrees of clinical benefit in different allergic indications including asthma, chronic spontaneous urticaria, atopic dermatitis, chronic rhinosinusitis with nasal polyps, food allergies and eosinophilic esophagitis. While multiple therapeutic antibodies have been approved for clinical use, scientists are still working on ways to improve on current treatment approaches. Here, we provide context to understand therapeutic targeting strategies and their limitations, discussing both knowledge gaps and promising future directions to enhancing clinical efficacy in allergic disease management.<\/jats:p>","DOI":"10.1111\/imr.13380","type":"journal-article","created":{"date-parts":[[2024,8,19]],"date-time":"2024-08-19T10:05:39Z","timestamp":1724061939000},"page":"387-411","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":77,"title":["Therapeutic monoclonal antibodies in allergy: Targeting\n                    <scp>IgE<\/scp>\n                    , cytokine, and alarmin pathways"],"prefix":"10.1111","volume":"328","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8746-3339","authenticated-orcid":false,"given":"Alexander","family":"Eggel","sequence":"first","affiliation":[{"name":"Department for BioMedical Research University of Bern  Bern Switzerland"},{"name":"Department of Rheumatology and Immunology University Hospital Bern  Bern Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7947-8714","authenticated-orcid":false,"given":"Luke F.","family":"Pennington","sequence":"additional","affiliation":[{"name":"Excellergy Inc.  San Jose California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3664-0072","authenticated-orcid":false,"given":"Theodore S.","family":"Jardetzky","sequence":"additional","affiliation":[{"name":"Department of Structural Biology Stanford University School of Medicine  Stanford California 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