BACKGROUND: TRALI may be a severe reaction associated with transfusion of plasma-containing blood components. TRALI has usually been associated with antibodies against granulocytes and HLA class I antigens, but more recently with antibodies against HLA class II and monocytes. TRALI cases were investigated to determine correlation between antigen and antibody. Additionally, activation of monocytes by TRALI serums was studied. STUDY DESIGN AND METHODS: Sixteen cases of TRALI were investigated. All patients were typed for HLA antigens. Implicated donors were screened for HLA antigens and antibodies against granulocytes and monocytes. In 6 cases, recipient monocyte activation was measured in vitro after incubation with TRALI and control serums. In four cases, monocyte activation was measured after incubation of TRALI serums against a panel of monocytes of known HLA antigen type. RESULTS: In 14 of the 16 cases (87.5%), antigen-antibody correlation was identified. TRALI monocytes, incubated with implicated TRALI serum (n = 6), expressed significantly greater cytokine and tissue factor (p < 0.05, repeated-measures ANOVA) than controls. Panel monocytes incubated with TRALI serum showed increased expression of cytokine and/or tissue factor when corresponding antigen was present. CONCLUSION: In most cases of TRALI, a correlation between antigen and antibody can be identified. Activation of monocytes and their subsequent release of cytokines may play a role in the pathogenesis of TRALI.
BACKGROUND: TRALI may be a severe reaction associated with transfusion of plasma-containing blood components. TRALI has usually been associated with antibodies against granulocytes and HLA class I antigens, but more recently with antibodies against HLA class II and monocytes. TRALI cases were investigated to determine correlation between antigen and antibody. Additionally, activation of monocytes by TRALI serums was studied. STUDY DESIGN AND METHODS: Sixteen cases of TRALI were investigated. All patients were typed for HLA antigens. Implicated donors were screened for HLA antigens and antibodies against granulocytes and monocytes. In 6 cases, recipient monocyte activation was measured in vitro after incubation with TRALI and control serums. In four cases, monocyte activation was measured after incubation of TRALI serums against a panel of monocytes of known HLA antigen type. RESULTS: In 14 of the 16 cases (87.5%), antigen-antibody correlation was identified. TRALI monocytes, incubated with implicated TRALI serum (n = 6), expressed significantly greater cytokine and tissue factor (p < 0.05, repeated-measures ANOVA) than controls. Panel monocytes incubated with TRALI serum showed increased expression of cytokine and/or tissue factor when corresponding antigen was present. CONCLUSION: In most cases of TRALI, a correlation between antigen and antibody can be identified. Activation of monocytes and their subsequent release of cytokines may play a role in the pathogenesis of TRALI.
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