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Immunologic Basis of Type 2 Biologics for Severe Asthma

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dc.contributor.authorSim, S-
dc.contributor.authorChoi, Y-
dc.contributor.authorPark, HS-
dc.date.accessioned2023-02-21T04:34:06Z-
dc.date.available2023-02-21T04:34:06Z-
dc.date.issued2022-
dc.identifier.issn1598-2629-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/24792-
dc.description.abstractAsthma is a chronic airway inflammatory disease characterized by reversible airway obstruction and airway hyperreactivity to various environmental stimuli, leading to recurrent cough, dyspnea, and wheezing episodes. Regarding inflammatory mechanisms, type 2/eosinophilic inflammation along with activated mast cells is the major one; however, diverse mechanisms, including structural cells-derived and non-type 2/neutrophilic inflammations are involved, presenting heterogenous phenotypes. Although most asthmatic patients could be properly controlled by the guided treatment, patients with severe asthma (SA; classified as a treatment-refractory group) suffer from uncontrolled symptoms with frequent asthma exacerbations even on regular anti-inflammatory medications, raising needs for additional controllers, including biologics that target specific molecules found in asthmatic airway, and achieving the precision medicine for asthma. This review summarizes the immunologic basis of airway inflammatory mechanisms and current biologics for SA in order to address unmet needs for future targets.-
dc.language.isoen-
dc.titleImmunologic Basis of Type 2 Biologics for Severe Asthma-
dc.typeArticle-
dc.identifier.pmid36627938-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9807964-
dc.subject.keywordAsthma-
dc.subject.keywordBiologics-
dc.subject.keywordEosinophils-
dc.subject.keywordInflammation-
dc.subject.keywordPhenotype-
dc.subject.keywordPrecision medicine-
dc.contributor.affiliatedAuthorChoi, Y-
dc.contributor.affiliatedAuthorPark, HS-
dc.type.localJournal Papers-
dc.identifier.doi10.4110/in.2022.22.e45-
dc.citation.titleImmune network-
dc.citation.volume22-
dc.citation.number6-
dc.citation.date2022-
dc.citation.startPagee45-
dc.citation.endPagee45-
dc.identifier.bibliographicCitationImmune network, 22(6). : e45-e45, 2022-
dc.identifier.eissn2092-6685-
dc.relation.journalidJ015982629-
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Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
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