Anti-JMH alloantibody in inherited JMH-negative patients leads to immunogenic destruction of JMH-positive RBCs

Autor:	Xiaojie Chen, Hui-Ying Huang, Xinxin Tong, Shufei He, Ming-Lu Zhong, Zhaohu Yuan, Xuexin Yang, Ya-Ming Wei, Zhen Liu, Kui Cai
Rok vydání:	2021
Předmět:	Adult CD4-Positive T-Lymphocytes Male 0301 basic medicine Erythrocytes Blood transfusion medicine.medical_treatment Immunology Population Antigen presentation Semaphorins Flow cytometry Interferon-gamma Mice 03 medical and health sciences 0302 clinical medicine Antigens CD Isoantibodies Interferon medicine Animals Humans Immunology and Allergy education Sensitization Autoantibodies Mice Knockout education.field_of_study medicine.diagnostic_test business.industry Autoantibody Original Articles Complement C3 Flow Cytometry Haemolysis Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure Antibody Formation Female business 030215 immunology medicine.drug
Zdroj:	Clin Exp Immunol
ISSN:	1365-2249 0009-9104
DOI:	10.1111/cei.13622
Popis:	Summary The clinical significance of the specific anti-John Milton Hagen (JMH) alloantibody in inherited JMH-negative patients remains unclear. During clinical blood transfusion, it is often classified as an anti-JMH autoantibody in acquired JMH-negative patients, which might further lead to the occurrence of haemolysis events. In this study, we found that the proportion of inherited JMH-negative people in the Guangzhou population was 0.41%, based on the study of 243 blood samples by flow cytometry. Gene sequencing analysis revealed two novel variants located in exon 11 (c.1348G>A, p.Ala449Thr) and exon 14 (c.1989G>T, p.Leu663Phe). Specific antigen presentation showed that JMH-positive RBCs (red blood cells) could be internalized by SEMA7A−/− dendritic cells (DCs) and that SEMA7A−/− DCs activated by the semaphorin 7a (Sema7a) protein or JMH-positive erythrocytes further induced activation of CD4+ T cells to secrete interferon (IFN)-γ. Transfusion of JMH-positive RBCs could lead to the production of the specific anti-JMH alloantibody in Sema7a knock-out (KO) C57 mice. After erythrocyte sensitization, complement C3 was specifically fixed, causing the destruction of JMH-positive erythrocytes. The anti-JMH alloantibody caused immunological destruction of JMH-positive erythrocytes and promoted the clearance of JMH-positive RBCs. We should be cautious when making conclusions about the clinical significance of the anti-JMH alloantibody.
Databáze:	OpenAIRE
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