Tumor necrosis factor-α augments the pro-inflammatory interaction between PMN and GBM via a CD 18 dependent mechanism-Reference-Cited by-同舟云学术

Tumor necrosis factor-α augments the pro-inflammatory interaction between PMN and GBM via a CD 18 dependent mechanism

Published:1995-09 Issue:3 Volume:48 Page:698-704
ISSN:0085-2538
Container-title:Kidney International
language:en
Short-container-title:Kidney International

Author:

Donovan Kieron L.,Coles Gerald A.,Williams John D.

Publisher

Elsevier BV

Subject

Nephrology

Reference33 articles.

1. Polymorphs infiltrate glomeruli in mesangial IgA glomerulonephritis;Kincaid-Smith;Kidney Int,1989

2. Relevance of experimental models for human nephropathy;Hoedemaeker;Kidney Int,1989

3. Mechanisms of glomerular injury in immune-complex disease;Couser;Kidney Int,1985

4. The renal glomerulus-the structural basis of ultrafiltration;Elger,1992

5. Lysosomal enzymes in human urine: Evidence for polymorphonuclear leucocyte proteinase involvement in the pathogenesis of human glomerulonephritis;Sanders;Clin Sci Mol Med,1978

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2. Pre-Existing Glomerular Immune Complexes Induce Polymorphonuclear Cell Recruitment Through an Fc Receptor-Dependent Respiratory Burst: Potential Role in the Perpetuation of Immune Nephritis;The Journal of Immunology;2003-03-15

3. Priming of neutrophils with tumor necrosis factor-α measured as Fcγ receptor-mediated respiratory burst correlates with increased complement receptor 3 membrane density;International Journal of Clinical & Laboratory Research;1996-12