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4 edition of Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment found in the catalog.

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment

Caius Kim

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment

by Caius Kim

  • 251 Want to read
  • 28 Currently reading

Published by National Library of Canada = Bibliothèque nationale du Canada in Ottawa .
Written in English


Edition Notes

SeriesCanadian theses = Thèses canadiennes
The Physical Object
FormatMicroform
Pagination1 microfiche : negative.
ID Numbers
Open LibraryOL14730501M
ISBN 10031574068X
OCLC/WorldCa30071509

  Kim C, Siminovitch KA, Ochi A: Reduction of lupus nephritis in MRL/Ipr mice by a bacterial superantigen treatment. J Exp Med , C Kim, KA Siminovitch, A OchiReduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. J Exp Med, (), pp.   T cells in lupus nephritis. MRL/lpr mice with B cells which are capable of expressing surface Ig, but not of secreting Ig, develop interstitial nephritis, rather than glomerulonephritis. This suggests the existence of another amplification loop in which B lymphocytes act as antigen-presenting cells in order to activate T cells.

  Similarly, treatment of lupus prone mice with Stattic decreased lymphoaccumulation and lymphadenopathy. Specifically, this treatment decreased the absolute numbers of T cells in MRL/lpr mice, without altering the relative frequencies of CD4 +, CD8 + and CD4 − CD8 − T cells. Stattic treatment also decreased the number of Tfh cells (CD4 + PD. Successful treatment of lupus nephritis in MRL-lpr/lpr mice by inhib-iting ornithine decarboxylase. Ornithine decarboxylase (ODC) is a key enzyme in the biosynthesis of cellular polyamines, putrescine, spermi-dine and spermine. Difluoromethylornithine (DFMO) is an irreversible inhibitor of ODC and thereby depletes putrescine and spermidine levels.

Treatment of MRL lpr/lpr mice with an anti-IL-3 mAb ameliorated nephritis, improved kidney function, and restrained production of certain autoantibodies (). This suggests that the IL . Lupus nephritis (LN) remains a major cause of ESRD and is associated with a >4-fold increase in mortality and significant morbidity in patients with lupus. The treatment of LN has evolved significantly over the past decade due to data from well conducted randomized controlled trials. We are currently in an era in which effective regimens exist in the form of induction and .


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Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment by Caius Kim Download PDF EPUB FB2

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. Rather than causing the expansion of V beta 8+ T cells, SEB administration resulted in the reduction V beta 8+, CD4-CD8- "double-negative" (DN) T cells.

Clonal diversity and T-cell receptor beta-chain variable gene expression in enlarged lymph nodes of Cited by:   Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

C Kim Division of Neurobiology and Molecular Immunology, Samuel S. Lunenfeld Research Instiute, Mount Sinai Hospital, Toronto, Ontario, by: Reduction of lupus nephritis in MRL/1pr mice by a bacterial superantigen treatment Article (PDF Available) in Journal of Experimental Medicine (6) January with 20 Reads.

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. J Exp Med 1 December ; (6): – doi: Thus, disease suppression was associated with a specific reduction in the number of V beta 8+, DN T Cited by: Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

The symptoms of systemic lupus erythematosus (SLE) in MRL/lpr, which include high titers of anti-DNA antibodies and circulating immune complexes and proteinuria, were reduced in SEB-treated mice in a dose- dependent manner.

Thus, disease. However, unlike other lupus models (e.g. NZB/NZW F1 discussed below), nephritis in MRL lpr mice is independent of FcγRs so the models relevance to human lupus may not be totally appropriate.

Nevertheless, inhibition of the monocyte chemokine CCL2/MCP-1 reduces LN pathology indicating macrophage recruitment is a key mechanism of autoimmune.

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. Kim, C., Siminovitch, K.A., Ochi, A. Exp. Med. () [ Pubmed ] The role of interleukin 12 and nitric oxide in the development of spontaneous autoimmune disease in MRL/MP-lpr/lpr mice.

Takahashi S., Nose M., Sasaki J., Yamamoto T. and Kyogoku M. () IgG3 production in MRL/lpr mice is responsible for development of lupus nephritis. Immunol. – PubMed Google Scholar. Kim C, Siminovitch KA, Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

J Exp Med. Dec 1; (6)– [ PMC free article ]. Experimental allergic encephalomyelitis (EAE), an antigen induced autoimmune disease, is mediated by Vβ8+ CD4+ T cells in PL/J mice after injection wi. Suppression of lupus nephritis and skin lesions in MRL/lpr mice by administration of the topoisomerase I inhibitor irinotecan Andreas Keil1, Sean R.

Hall1, Meike Körner2, Martin Herrmann3, Ralph A. Schmid1 and Steffen Frese1* Abstract Background: Since the precise mechanism for the pathogenesis of systemic lupus erythematosus (SLE) is unknown.

Lupus-prone mouse model SNF1: A higher abundance of the Rikenellaceae family of commensal bacteria was found to be associated with more severe SLE-like disease. Lactobacillus spp. MRL/lpr mice-Ameliorating lupus nephritis. Bifidobacterium bifidum LMG In vitro cultures with fecal microbiota isolated from SLE patients.

Kim C, Siminovitch KA, Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. J Exp Med. Dec 1; (6)– [PMC free article] Kotzin BL, Babcock SK, Herron LR.

Deletion of potentially self-reactive T cell receptor specificities in L3T4- Lyt T cells of lpr mice. Kim C, Siminovitch KA, Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

J Exp Med. Dec 1; (6)– [Europe PMC free article] [Google Scholar] Kotzin BL, Babcock SK, Herron LR. Deletion of potentially self-reactive T cell receptor specificities in L3T4- Lyt T cells of lpr mice.

Bacterial lipopolysaccharide transforms mesangial into proliferative lupus nephritis without interfering with processing of pathogenic immune complexes in NZB/W mice. Am J Pathol. Oct; (4)– [PMC free article] Kim C, Siminovitch KA, Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

Mice homozygous for the lymphoproliferation mutation (Fas lpr) exhibit autoimmune disease that closely resembles human systemic lupus erythematosus (SLE). Induction. Spontaneous onset. Disease Parameters/Progression.

Systemic autoimmunity, lymphadenopathy associated with proliferation of aberrant T cells, immune complex glomerulonephritis and arthritis start at. E ff ects of bacterial superantigen and lupus nephritis the ment of autoimmune glomerulonephritis in MRL / lpr mice.

This reduction was accompanied by genomic DNA fragmentation that. microbiota of lupus-prone lpr mice vs. MRL control mice, we found that female lpr mice had a significantly lower abundance of Lactobacillales in the gut microbiota than MRL controls at 5 weeks of age and prior to the onset of lupus-like disease (Additional file 1: Figure S1A).

However, it was unclear whether the change was a. Lactobacillus spp. attenuate LN. When comparing the bacterial composition in the gut microbiota of lupus-prone lpr mice vs.

MRL control mice, we found that female lpr mice had a significantly lower abundance of Lactobacillales in the gut microbiota than MRL controls at 5 weeks of age and prior to the onset of lupus-like disease (Additional file 1: Figure S1A). To test the potential protective effects of CTLA4/IgG gene delivery on the development of lupus nephritis, these investigators injected MRL lpr/lpr mice with a recombinant adenovirus vector.

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. Spontaneous elaboration of transforming growth factor beta suppresses host defense against bacterial infection in autoimmune MRL/lpr mice.This strain is commonly known as MRL- lpr or lpr mutant.

Mice are homozygous for the lymphoproliferation spontaneous mutation (Fas lpr), and show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Mice are useful as a model to determine the etiology of systemic lupus .Jevnikar AM, Grusby MJ, Glimcher LH.

Prevention of nephritis in major histocompatibility complex class II-deficient MRL-lpr mice. J Exp Med. Apr 1; (4)– [PMC free article] Kim C, Siminovitch KA, Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

J Exp Med. Dec 1; (6)