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Functional Characterization of Regulatory Macrophages That Inhibit Graft-reactive Immunity
Published on: June 7, 2017
Expression of HLA-DR in granulocytes of polytraumatized patients treated with recombinant human granulocyte
G C Spagnoli1, A Juretic, R Rosso
1Department of Surgery, University of Basel, Switzerland.
MHC class II determinants are the restriction elements involved in antigen-specific activation of helper T lymphocytes and interaction with CD4 molecules. They are typically expressed on a limited number of cell types, mostly endowed with antigen-presenting capacity. Recently, expression of HLA-DR has been detected on granulocytes stimulated "in vitro" with GM-CSF. However, no evidence of "in vivo" expression in humans has been presented so far. We report here that class II determinant expression is detectable in vivo on peripheral blood granulocytes of polytraumatized patients upon intravenous administration of rhGM-CSF. Expression of these molecules appears to be an early effect of rhGM-CSF treatment, independent from endotoxemia or endogenous production of IL-6 or TNF-alpha, and rapidly declining upon discontinuation of therapy. Thus, this treatment might increase the number of cells potentially capable of presenting class-II-restricted antigens in these patients.
MHC class II determinants are the restriction elements involved in antigen-specific activation of helper T lymphocytes and interaction with CD4 molecules. They are typically expressed on a limited number of cell types, mostly endowed with antigen-presenting capacity. Recently, expression of HLA-DR has been detected on granulocytes stimulated "in vitro" with GM-CSF. However, no evidence of "in vivo" expression in humans has been presented so far. We report here that class II determinant expression is detectable in vivo on peripheral blood granulocytes of polytraumatized patients upon intravenous administration of rhGM-CSF. Expression of these molecules appears to be an early effect of rhGM-CSF treatment, independent from endotoxemia or endogenous production of IL-6 or TNF-alpha, and rapidly declining upon discontinuation of therapy. Thus, this treatment might increase the number of cells potentially capable of presenting class-II-restricted antigens in these patients.
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