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TNF‐specific deactivation of granulocytes in vivo: A possible mechanism of self‐protection
Author(s) -
Schleiffenbaum Boris,
Olgiati Licia,
Fehr Jorg
Publication year - 1992
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1992.tb00055.x
Subject(s) - tumor necrosis factor alpha , in vivo , chemistry , complement system , in vitro , receptor , exocytosis , immunology , granulocyte , respiratory burst , microbiology and biotechnology , secretion , biochemistry , biology , immune system
Granulocytes (PMN) have recently been shown to be specifically deactivated towards tumor necrosis factor (TNF) by preexposure to TNF itself and to other stimuli such as endotoxin and complement C5a in vitro. When TNF (200 μg/m 2 ) was infused to a male volunteer, we found ex vivo an almost complete TNF‐specific deactivation of PMN adhesion (57 ± 3* vs 6 ± 2%**), of exocytosis of secondary granules (37 ± 1* vs 7 ± 1%**) and of the respiratory burst as measured by hexose monophosphate shunt activation (74 ± 1* vs 12 ± 3** nM/10 7 PMN/45 min). Furthermore, up‐ and down‐regulation, respectively, of the PMN surface adhesion molecules Mac‐1 and LAM‐1 became TNF‐resistant. Similar to the results obtained in vitro , deactivation correlated with a decrease in the number of cellular TNF receptors. In PMN of 4 patients exposed to activated complement during hemodialysis, a state of TNF‐specific cross‐deactivation could also be demonstrated.