دورية أكاديمية
أعرض في EDS

Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.

التفاصيل البيبلوغرافية
العنوان: Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.
المؤلفون: Kulkarni HS
المصدر: The Journal of clinical investigation [J Clin Invest] 2024 Jun 03; Vol. 134 (11). Date of Electronic Publication: 2024 Jun 03.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 7802877 Publication Model: Electronic Cited Medium: Internet ISSN: 1558-8238 (Electronic) Linking ISSN: 00219738 NLM ISO Abbreviation: J Clin Invest Subsets: MEDLINE
أسماء مطبوعة: Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation
Original Publication: New Haven [etc.] American Society for Clinical Investigation.
مواضيع طبية MeSH: Immunoglobulin G*/immunology , Acute Lung Injury*/immunology , Acute Lung Injury*/pathology , Complement Activation*/immunology, Humans ; Animals ; Isoantibodies/immunology ; Protein Multimerization/immunology ; Histocompatibility Antigens Class I/immunology ; Antigen-Antibody Complex/immunology
مستخلص: Although antibody-mediated lung damage is a major factor in transfusion-related acute lung injury (ALI), autoimmune lung disease (for example, coatomer subunit α [COPA] syndrome), and primary graft dysfunction following lung transplantation, the mechanism by which antigen-antibody complexes activate complement to induce lung damage remains unclear. In this issue of the JCI, Cleary and colleagues utilized several approaches to demonstrate that IgG forms hexamers with MHC class I alloantibodies. This hexamerization served as a key pathophysiological mechanism in alloimmune lung injury models and was mediated through the classical pathway of complement activation. Additionally, the authors provided avenues for exploring therapeutics for this currently hard-to-treat clinical entity that has several etiologies but a potentially focused mechanism.
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معلومات مُعتمدة: K08 HL148510 United States HL NHLBI NIH HHS; R01 HL166449 United States HL NHLBI NIH HHS; R01 HL169860 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Immunoglobulin G)
0 (Isoantibodies)
0 (Histocompatibility Antigens Class I)
0 (Antigen-Antibody Complex)
تواريخ الأحداث: Date Created: 20240603 Date Completed: 20240603 Latest Revision: 20240607
رمز التحديث: 20240607
مُعرف محوري في PubMed: PMC11142731
DOI: 10.1172/JCI181137
PMID: 38828725
قاعدة البيانات: MEDLINE
الوصف
تدمد:1558-8238
DOI:10.1172/JCI181137