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Transfusion‐related acute lung injury caused by human leucocyte antigen class II antibody
Author(s) -
Flesch Brigitte K.,
Neppert Jürgen
Publication year - 2002
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.0007-1048.2001.03305.x
Subject(s) - immunology , antibody , medicine , antigen , monocyte , transfusion related acute lung injury , phagocytosis , fc receptor , cytotoxic t cell , human leukocyte antigen , in vivo , lung , in vitro , chemistry , biology , pulmonary edema , biochemistry , microbiology and biotechnology
Summary. Fcγ receptor (FcγR)‐mediated destruction of immunoglobulin‐coated red blood cells (RBCs) is the underlying mechanism of haemolytic disease of the newborn. Human leucocyte antigen (HLA) antibodies in vitro are able to block monocyte FcγRs and prevent phagocytosis. The intention was to demonstrate this effect in vivo upon a volunteer. Plasma containing a non‐cytotoxic HLA‐DR alloantibody was infused into the subject. The FcγR blockade was achieved and persisted for about 2·5 d, but, unexpectedly, a mild transfusion‐related acute lung injury (TRALI) was also caused. Monocytes disappeared completely from the peripheral blood within the first hour after infusion and a mild pulmonary oedema was observed within 3–4 h. The subject recovered within 2 d.