BACKGROUND: ABO antigen-antibody interaction in the presence of periph
eral blood leukocytes (white cells) results in the production of a var
iety of proinflammatory cytokines. However, although tumor necrosis fa
ctor cr has been shown to be derived al least primarily from monocytes
, the range of cells activated by this process has not previously been
reported. Therefore, changes in mononuclear cell surface antigen expr
ession were studied, to determine which subsets of white cells appeare
d to be activated in the setting of ABO incompatibility.STUDY DESIGN A
ND METHODS: Group O peripheral blood mononuclear cells (PBMCs) were in
cubated in autologous plasma with group A or O red cells (RBCs) for up
to 24 hours. White cell expression of activation and adhesion markers
was measured at 2 and 24 hours by flow cytometry, using direct or ind
irect fluorescein or phycoerythrin labeling. RESULTS: Expression of ly
mphocyte activation markers CD25, GDw108, and CD109 was equivalent whe
n PBMCs incubated with group A and O RBCs were compared. However, afte
r 2 hours, mean fluorescence of CD14 on PBMCs incubated with group A R
BCs was 65 percent of that on PBMCs incubated with group O RBCs and re
mained similarly decreased at 24 hours. CD44 expression was upregulate
d on PBMCs exposed to both group A and O RBCs, but it was increased si
gnificantly more on monocytes exposed to group A RBCs. The ability to
bind hyaluronic acid was induced in approximately 42 percent of CD14monocytes exposed to group A RBCs but in no cells exposed to group O R
BCs. CONCLUSION: Downregulation of CD14 and increased binding of hyalu
ronic acid reflects monocyte activation in this model. No evidence of
lymphocyte activation was found, supporting the hypothesis that ABO tr
ansfusion reactions primarily activate monocytes.