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Role of anti‐human leucocyte antigen class II alloantibody and monocytes in development of transfusion‐related acute lung injury
Author(s) -
Nishimura M.,
Hashimoto S.,
Takanashi M.,
Okazaki H.,
Satake M.,
Nakajima K.
Publication year - 2007
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1111/j.1365-3148.2006.00721.x
Subject(s) - transfusion related acute lung injury , human leukocyte antigen , immunology , monocyte , antibody , antigen , medicine , lung , pulmonary edema
summary Recently, evidence implicating the roles of the anti‐human leucocyte antigen (HLA) class II antibody in the development of transfusion‐related acute lung injury (TRALI), which is one of the most serious possible side effects of transfusion, has been accumulating. The aim of this study is to clarify the roles of the anti‐HLA DR alloantibody in TRALI development. Cultured human lung microvascular endothelial (LME) cells were incubated with either HLA‐DR15‐positive or HLA‐DR15‐negative monocytes together with serum from a single multiparous donor previously implicated in a clinical case of TRALI and known to contain anti‐HLA DR15 antibody. Production of soluble leukotriene B 4 (LTB 4 ) was measured in the supernatant and found to be markedly increased in the presence of HLA‐DR15‐positive monocytes but not with the HLA‐DR15‐negative monocytes or in the absence of LME cells. The vascular cell adhesion molecule‐1 expression in LME cells and leucocyte‐function‐associated molecule‐1 (LFA‐1) expression in HLA‐DR15‐positive monocytes were notably enhanced after combined culture of LME cells, HLA‐DR15‐positive monocytes and TRALI‐inducing anti‐HLA DR15 antibody‐positive serum. In conclusion, anti‐HLA DR alloantibodies may be implicated in LME dysfunction that leads to TRALI, in a monocyte‐dependent manner.