PubMed · 3740644
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T M Daniel. 1986. Circulating immune complexes in tuberculosis.. https://doi.org/10.1164/arrd.1986.134.2.199
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Intracellular H2O2 generation, as a measure of the respiratory burst, was determined after stimulation of neutrophils by immune complex (IC)-bearing human umbilical vein endothelial cells. Under static conditions, neutrophils basically responded to the immune deposits on resting endothelial cells. The rotating shear forces of approximately 0.7 dynes/cm2, corresponding to the physiological flow in postcapillary venules, completely abolished this basal H2O2 generation. After activation of the IC-bearing endothelial layers with interleukin-1 (IL-1) or tumor necrosis factor (TNF), or both, for 4 hours, rolling adhesion of the neutrophils was induced, accompanied by considerable H2O2 production. The neutrophil respiratory burst was prominently inhibited by anti-FcgammaRIII MoAb 3G8 (72.4%), and partially by MoAb 2E1 against FcgammaRII (38.5%). Both MoAbs together inhibited the Fc-mediated H2O2 generation by 93. 4%. The respiratory burst and rolling adhesion were markedly blocked by MoAb LAM1-3 against L-selectin (91.3%), whereas the nonfunctional anti-L-selectin MoAb LAM1-14 was ineffective. F(ab)2' fragments of MoAb 7A9 against E-selectin inhibited neutrophil rolling by 98.6%, but not the respiratory burst. Moreover, rolling adhesion of neutrophils and the related oxidative burst were CD11b/CD18- independent. In summary, L-selectin has a unique auxiliary function in triggering the FcgammaR-mediated respiratory burst of rolling neutrophils to IC-bearing endothelial cells, thereby substituting CD11b/CD18 under conditions of flow.
BACKGROUND: Based on the histologic findings of fully developed lesions, leukocytoclastic vasculitis has been regarded as the histologic criterion for differentiating urticarial vasculitis from urticaria. Nevertheless, because the early lesions have not been examined histologically, the key biological events leading to the development of leukocytoclastic vasculitis remain unknown. To address this issue, urticarial vasculitis lesions induced by physical exercise were sequentially examined histologically and immunohistochemically in a patient over the course of 24 hours. Serum levels of various cytokines also were determined in parallel. OBSERVATIONS: At 3 hours after exercise challenge, the number of identifiable mast cells decreased and the first cell type that appeared around the vessels was the eosinophil. The serum tumor necrosis factor alpha level was strikingly increased as compared with that before challenge. Intense expression of E-selectin was also induced at 3 hours. The deposition of eosinophil peroxidase was observed at 3 hours and reached maximum deposition at 10 hours. The eosinophil peroxidase deposits preceded the prominent influx of neutrophils and the subsequent deposits of neutrophil elastase. CONCLUSION: The extracellular deposition of eosinophil granule proteins, in addition to the deposition of immune complexes and a variety of cytokines from the infiltrating cells, appears to be one of the key biological events that determines whether urticarial lesions resolve without causing vasculitis or develop into vasculitis.
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