Large doses of anti-glomerular basement membrane antibody (AGBM-Ab) have been shown consistently to decrease both single nephron filtration rate (SNGFR) and the glomerular ultrafiltration coefficient (LpA) within 60 min of administration of the antibody. Both the decrease in SNGFR and LpA may be the result of infiltration of leukocytes blocking capillary loops and/or endothelial cell separation from the glomerular basement membrane through leukocyte dependent activated cytotoxic products or by mechanisms associated with leukocyte activation and infiltration. Administration of 2.5 micrograms/g body wt AGBM-Ab was performed in 10 control Munich-Wistar rats and in six Munich-Wistar rats in which 3 to 5 days prior to micropuncture experiments the rats were splenectomized and then irradiated to produce leukocyte depletion. Micropuncture measurements were performed in a condition of plasma volume expansion both prior to and after AGBM-Ab administration. In the control group, SNGFR decreased from 64 +/- 3 to 48 +/- 2 nl/min X g kidney wt after AGBM-Ab administration due to a decrease in LpA from 0.13 to 0.06 nl X sec-1 X mm Hg-1 X g kidney wt-1. This decrease in either SNGFR or LpA did not occur in the leukocyte depleted group. Linear deposits of IgG and C3 were similar in both groups. Polymorphonuclear leukocytes were significantly decreased in glomerulus from 7.4 +/- 0.7 in control vs. 0.7 +/- 0.3 in leukocyte depletion (P less than 0.01). There was no difference in glomerular dynamics between controls and leukocyte depleted rats prior to AGBM-Ab administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1038/ki.1985.114 | DOI Listing |
JMIR Res Protoc
January 2025
Department of Orthopaedic Surgery, National University Hospital, National University Health System, Singapore, Singapore.
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January 2025
Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
The management of autoimmune diseases is currently limited by therapies that largely suppress the immune system, often resulting in partial and temporary remissions. Cellular immunotherapies offer a targeted approach by redirecting immune cells to correct the underlying autoimmunity. This review explores the latest advances in cellular immunotherapies for autoimmune diseases, focusing on various strategies, such as the use of chimeric antigen receptor (CAR) T cells, chimeric auto-antibody receptor (CAAR) T cells, regulatory T cells (Tregs), and tolerogenic dendritic cells (TolDCs).
View Article and Find Full Text PDFJ Clin Invest
January 2025
Division of Rheumatology, Center of Excellence for Intestinal and Immunology Research, University of Alberta, Edmonton, Alberta, Canada.
Superantigen-induced (Sag-induced) autoimmunity has been proposed as a mechanism for many human disorders, without a clear understanding of the potential triggers. In this issue of the JCI, McCarthy and colleagues used the SKG mouse model of rheumatoid arthritis to characterize the role of Sag activity in inflammatory arthritis by profiling arthritogenic naive CD4+ T cells. Within the diseased joints, they found a marked enrichment of T cell receptor-variable β (TCR-Vβ) subsets that were reactive to the endogenously encoded mouse mammary tumor virus (MMTV) Sag.
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Digestive Disease Center, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang Province, 154000, China.
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View Article and Find Full Text PDFBreast Cancer (Auckl)
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Background: Circulating rare cells participate in breast cancer evolution as systemic components of the disease and thus, are a source of theranostic information. Exploration of cancer-associated rare cells is in its infancy.
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