dc.contributor.author
Bartolmäs, Thilo
dc.contributor.author
Pruß, Axel
dc.contributor.author
Mayer, Beate
dc.date.accessioned
2023-09-12T13:07:41Z
dc.date.available
2023-09-12T13:07:41Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/40832
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-40553
dc.description.abstract
Antibodies to red blood cells (RBCs) may hemolyze erythrocytes via Fc-mediated phagocytosis or complement-dependent. Complement activation on RBCs can be detected by C3d-direct antiglobulin test (DAT), which is the only test in immune hematology that directly targets complement. However, a positive DAT with anti-C3d cannot distinguish between C3b-mediated extravascular hemolysis, C5b-C9-mediated intravascular hemolysis and C5b-C8-mediated eryptosis. Furthermore, DAT is not suitable to estimate the strength of hemolysis. Autoimmune hemolytic anemia (AIHA) is a rare disease that is caused by autoantibodies to red blood cells that is divided in warm AIHA and in cold agglutinin disease (CAD). The causative antibodies in CAD and sometimes in warm AIHA are from the IgM class. Depending on strength of complement activation they can induce extravascular hemolysis, intravascular hemolysis and eryptosis. We studied the three types of hemolysis by use of sera from patients with CAD under various conditions. We found that additionally to the routinely applied C3d-DAT, indirect tests for complement activity (free hemoglobin and Annexin V-binding to phosphatidylserine-exposing RBCs) should be used to determine the portion of extravascular, intravascular and eryptotic hemolysis. Eryptotic hemolysis may have a significant share in clinical relevant CAD or IgM warm AIHA, which should be considered for successful treatment.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
cold agglutinin
en
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Three different pathways of IgM-antibody-dependent hemolysis are mainly regulated by complement
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
1114509
dcterms.bibliographicCitation.doi
10.3389/fimmu.2023.1114509
dcterms.bibliographicCitation.journaltitle
Frontiers in Immunology
dcterms.bibliographicCitation.originalpublishername
Frontiers Media SA
dcterms.bibliographicCitation.volume
14
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
36817469
dcterms.isPartOf.eissn
1664-3224