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PMID: 765016 Published · ppublish English Journal Article

The role of polymorphonuclear leucocytes in the autologous phase of nephrotoxic nephritis.

Clinical and experimental immunology ·Vol. 22 ·No. 1 ·1975-10-00 ·Pages 102-11

Naish PF, Thomson NM, Simpson IJ, Peters DK

Abstract

The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.

MeSH Terms
Animals Antibodies/analysis Antilymphocyte Serum Complement C3/analysis Fibrin/metabolism Fluorescent Antibody Technique Kidney/physiopathology Kidney Glomerulus/immunology,pathology Leukocytes/drug effects Male Mechlorethamine/pharmacology Nephritis/immunology Neutrophils/immunology Proteinuria/etiology,immunology Rabbits
Chemicals
Antibodies Antilymphocyte Serum Complement C3 Mechlorethamine Fibrin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Naish P F
Thomson N M
Simpson I J
Peters D K
References (18)
18 references, click to expand
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Article Info
Journal
Clinical and experimental immunology
Abbr.
Clin Exp Immunol
ISSN
0009-9104
Published
1975-10-00
Pages
102-11
Language
English
Region
England
NLM ID
0057202
PMCID
PMC1538337
Subset
IM
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