Depletion of CD8 positive cells in nephrotoxic serum nephritis of WKY rats

Kawasaki, Keisuke; Yaoita, Eishin; Yamamoto, Tadashi; Kihara, Itaru

doi:10.1038/ki.1992.221

Cited by 156 publications

(144 citation statements)

References 32 publications

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“…The cellular sources of CC chemokines in this model are unknown. MIP-1a, MIP-1b and RANTES are produced mainly by T lymphocytes [38], and numbers of CD8 þ cells increase in glomeruli in this model at early stages ( [36], our unpublished observation). Therefore, CD8 + cells might be responsible for the early induction of these chemokines in the model.…”

Section: Discussionmentioning

confidence: 65%

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Natori¹,

Sekiguchi²,

Ou³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYCGN is a rapidly progressive glomerular disease. Monocytes/macrophages are frequently observed in glomeruli in cases of CGN and they are considered to play a crucial role in the pathogenesis of this disease. We described previously the glomerular expression of monocyte chemoattractant protein-1 (MCP-1), which is a potent chemoattractant for monocytes and a member of CC chemokine family, in an experimental model of CGN. In the present study we investigated the expression of mRNAs for other CC chemokines, namely, MCP-3, macrophage inflammatory protein-1a (MIP-1a), MIP-1b, RANTES and TCA3, all of which are chemotactic for monocytes, in the CGN model. First, we established a reverse transcriptase-polymerase chain reaction (RT-PCR) method by which mRNA for each of the CC chemokines could be amplified separately, and then we measured the levels of the expression of mRNAs for the chemokines in diseased glomeruli at several time points after induction of CGN. The mRNAs for all CC chemokines examined were expressed in glomeruli of rats with CGN. Moreover, induction of the gene expression of MIP-1a and MIP-1b seemed to occur earlier than that of the others. CC chemokines may contribute to the recruitment and activation of monocytes in CGN, and each individual CC chemokine may play an overlapping but distinct role in the pathogenesis of this disease.

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Section: Discussionmentioning

confidence: 65%

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Natori¹,

Sekiguchi²,

Ou³

et al. 1997

Clinical and Experimental Immunology

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“…This may explain the finding that vIL-10 did not repress perforin, which is produced by CD8 + T cells. A previous study demonstrated that CD8 + T cells play an important role in experimental crescentic GN; 40 however, pCAGGS-vIL-10 gene transfer exhibited therapeutic effects without an apparent suppression of CD8 + T cells.…”

Section: Discussionmentioning

confidence: 90%

Hydrodynamics-based delivery of the viral interleukin-10 gene suppresses experimental crescentic glomerulonephritis in Wistar–Kyoto rats

et al. 2003

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Gene therapy is expected to revolutionize the treatment of kidney diseases. Viral interleukin (vIL)-10 has a variety of immunomodulatory properties. We examined the applicability of vIL-10 gene transfer to the treatment of rats with crescentic glomerulonephritis, a T helper 1 (Th 1) predominant disease. To produce the disease, Wistar-Kyoto rats were injected with a rabbit polyclonal anti-rat glomerular basement membrane antibody. After 3 h, a large volume of plasmid DNA expressing vIL-10 (pCAGGS-vIL-10) solution was rapidly injected into the tail vein. pCAGGS solution was similarly injected into control rats (pCAGGS rats). We confirmed the presence of vector-derived vIL-10 mainly in the liver and observed high serum vIL-10 levels in pCAGGSvIL-10-injected rats. Compared with the pCAGGS rats, the pCAGGS-vIL-10 rats showed significant therapeutic effects: reduced frequency of crescent formation, decrease in the number of total cells, macrophages, and CD4 + T cells in the glomeruli, decrease in urine protein, and attenuation of kidney dysfunction. Using quantitative real-time polymerase chain reaction, we also observed that this model was Th1-predominant in the glomeruli and that the ratio of the transcripts of CD4, interferon-g, tumor necrosis factor-a, and monocyte chemotactic protein-1 to the transcripts of glucose-6-phosphate dehydrogenase in the glomeruli were all significantly lower in the pCAGGS-vIL-10 rats than in the pCAGGS rats. These results demonstrate that pCAGGS-vIL-10 gene transfer by hydrodynamics-based transfection suppresses crescentic glomerulonephritis.

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“…The peak influx of Mo/M occurs later (days 6 and 11) than that of CD8 ϩ cells (day 3). 35 In this study we investigated the role of MDC, a novel C-C chemokine for monocytes, activated lymphocytes, dendritic cells, and NK cells in the development of this model of GN. We first examined MDC expression in the glomeruli during the evolution of the lesion and then established its functional role with blocking Ab.…”

Section: Discussionmentioning

confidence: 99%

“…MDC riboprobe was synthesized with incorporation of 35 S-UTP as previously described. 10 Following in situ hybridization and before dehydration, the slides were incubated for 5 minutes in Tris-buffered saline.…”

Section: In Situ Hybridization and Immunohistochemistrymentioning

confidence: 99%

“…35,36 In this model of GN, enhanced gene expression of chemokines has been demonstrated; however, most of the studies have focused on the acute phase of the disease. 13,37 Furthermore, studies with neutralizing antibodies and blocking reagents targeted acute glomerular injury and were used at day l, or at the same time as anti-GBM Ab administration, before the development of the disease.…”

mentioning

confidence: 99%

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Mononuclear Cell-Infiltrate Inhibition by Blocking Macrophage-Derived Chemokine Results in Attenuation of Developing Crescentic Glomerulonephritis

García

Xia

Harrison

et al. 2003

The American Journal of Pathology

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Depletion of CD8 positive cells in nephrotoxic serum nephritis of WKY rats

Cited by 156 publications

References 32 publications

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Hydrodynamics-based delivery of the viral interleukin-10 gene suppresses experimental crescentic glomerulonephritis in Wistar–Kyoto rats

Mononuclear Cell-Infiltrate Inhibition by Blocking Macrophage-Derived Chemokine Results in Attenuation of Developing Crescentic Glomerulonephritis

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