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Depending on the underlying pathology, molecular defect(s), and the cytokine- and mediator-cascades involved, peripheral blood and tissue hypereosinophilia (HE) may develop and may lead to organ dysfunction or even organ damage which usually leads to the diagnosis of a HE syndrome (HES). In some of these patients, the etiology and impact of HE remain unclear. These patients are diagnosed with idiopathic HE. In other patients, HES is diagnosed but the etiology remains unknown \u2014 these patients are classified as idiopathic HES. For patients with HES, early therapeutic application of agents reducing eosinophil counts is usually effective in avoiding irreversible organ damage. Therefore, it is important to systematically explore various diagnostic markers and to correctly identify the disease elicitors and etiology. Depending on the presence and type of underlying disease, HES are classified into primary (clonal) HES, reactive HES, and idiopathic HES. In most of these patients, effective therapies can be administered. The current article provides an overview of the pathogenesis of eosinophil-associated disorders, with special emphasis on the molecular, immunological, and clinical complexity of HE and HES. In addition, diagnostic criteria and the classification of eosinophil disorders are reviewed in light of new developments in the field.<\/jats:p>","DOI":"10.1007\/s00281-021-00863-y","type":"journal-article","created":{"date-parts":[[2021,6,29]],"date-time":"2021-06-29T18:02:48Z","timestamp":1624989768000},"page":"423-438","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":68,"title":["Eosinophils and eosinophil-associated disorders: immunological, clinical, and molecular complexity"],"prefix":"10.1007","volume":"43","author":[{"given":"Peter","family":"Valent","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lina","family":"Degenfeld-Schonburg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irina","family":"Sadovnik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Peter","family":"Horny","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michel","family":"Arock","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Uwe","family":"Simon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Reiter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce S.","family":"Bochner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,5,30]]},"reference":[{"issue":"4","key":"863_CR1","doi-asserted-by":"publisher","first-page":"651","DOI":"10.1067\/mai.2000.105712","volume":"105","author":"GJ Gleich","year":"2000","unstructured":"Gleich GJ (2000) Mechanisms of eosinophil-associated inflammation. 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The authors declare the following conflicts of interest outside of this project: P.V. received a research grant from Pfizer, Celgene, and Novartis, and consultancy-related honoraria from Novartis, Pfizer, Celgene, Blueprint, Incyte, Abbvie, AB Science, Accord, Alexion, Orphan Pharmaceuticals, and TLL The Longevity Labs. H.U.S. is a consultant for GlaxoSmithKline. A.R. received consultancy honoraria from Novartis, Incyte, GSK, Astra Zeneca, Blueprint, Celgene\/BMS, and Abbvie. B.S.B. receives publication-related royalty payments from Elsevier and UpToDate. He receives remuneration for consulting services (Blueprint Medicine, Glaxo SmithKline, Sanofi\/Regeneron) and for serving on the scientific advisory board of Third Harmonic Bio. He also receives remuneration for serving on the scientific advisory board of Allakos, which he co-founded, and owns stock in Allakos. He is a co-inventor on existing Siglec-8-related patents and thus may be entitled to a share of royalties received by Johns Hopkins University during development and potential sales of such products. The terms of this arrangement are being managed by Johns Hopkins University and Northwestern University in accordance with their conflict of interest policies.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}