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4 results on '"Kohei Nagasawa"'

1. Phenotyping of P105-Negative B Cell Subsets in Patients with Systemic Lupus Erythematosus

Author

Syuichi Koarada, Yoshifumi Tada, Rie Suematsu, Sachiko Soejima, Hisako Inoue, Akihide Ohta, and Kohei Nagasawa

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

This study aimed to investigate phenotype of RP105(−) B cell subsets in patients with systemic lupus erythematosus (SLE). Flow cytometry was used for phenotyping RP105-negaive B cell subsets. Based on CD19, RP105, and CD138 expression, RP105(−) B cells consist of at least 5 subsets of late B cells, including CD19(+)RP105(int), CD19(+) RP105(−), CD19(low) RP105(−) CD138(−), CD19(low) RP105(−)CD138(int), and CD19(low) RP105(−) CD138(++) B cells. Especially, CD19(+)RP105(int) and CD19(low) RP105(−)CD138(int) B cells are significantly larger than other RP105(−) B cell subsets in SLE. By comparison of RP105(−) B cell subsets between patients with SLE and normal subjects, these subsets were detectable even in normal subjects, but the percentages of RP105(−) B cell subsets were significantly larger in SLE. The phenotypic analysis of RP105(−) B cell subsets suggests dysregulation of later B cell subsets in SLE and may provide new insights into understanding regulation of B cells in human SLE.

Published
2012
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2. Interferon regulatory factor 5 is critical for the development of lupus in MRL/lpr mice

Author

Rie Suematsu, Seiji Kondo, Akihide Ohta, Tak W. Mak, Yoshifumi Tada, Shigehisa Aoki, Syuichi Koarada, Kohei Nagasawa, and Hisako Inoue

Subjects
CD4-Positive T-Lymphocytes, Male, Mice, Inbred MRL lpr, Immunology, urologic and male genital diseases, Mice, Glomerulonephritis, Immune system, Rheumatology, Antigen, Risk Factors, immune system diseases, Animals, Humans, Lupus Erythematosus, Systemic, Immunology and Allergy, Medicine, Genetic Predisposition to Disease, Pharmacology (medical), skin and connective tissue diseases, Autoantibodies, Mice, Knockout, Membrane Glycoproteins, Lupus erythematosus, Systemic lupus erythematosus, business.industry, Homozygote, Autoantibody, Dendritic Cells, Dendritic cell, medicine.disease, Disease Models, Animal, Toll-Like Receptor 7, Toll-Like Receptor 9, Interferon Regulatory Factors, Female, business, IRF5, Interferon regulatory factors
Abstract

Objective Interferon regulatory factor 5 (IRF-5) is a transcription factor that mediates intracellular signals activated by engagement of Toll-like receptors (TLRs). IRF5 polymorphisms are associated with an increased or decreased risk of systemic lupus erythematosus (SLE) in various human populations, but the precise role of IRF5 in SLE development is not fully understood. This study was undertaken to examine the role of IRF5 in the development of murine lupus. Methods We crossed gene-targeted IRF5-deficient (IRF5−/−) mice with MRL/MpJ-lpr/lpr (MRL/lpr) mice and examined the progeny for survival, glomerulonephritis, autoantibody levels, immune system cell populations, and dendritic cell function. Results IRF5−/−MRL/lpr mice survived longer than control IRF5+/+MRL/lpr mice and displayed only very mild glomerulonephritis. Autoantibodies to SLE-related nuclear antigens were lower in IRF5−/−MRL/lpr mouse serum, and numbers of activated CD4+ T cells were reduced in the spleen. Splenic DCs from IRF5−/−MRL/lpr mice produced lower levels of inflammatory cytokines when treated in vitro with TLR-7 or TLR-9 ligands or immune complexes. Interferon-α production in response to CpG was also decreased. Conclusion Our results show that IRF5 is a crucial driver of lupus development in mice, and indicate that IRF5 may be an attractive new target for therapeutic intervention to control disease in SLE patients.

Published
2011

4. Production of the third and fourth component of complement (C3, C4) by smooth muscle cells

Author

Hiroaki Nishizaka, Hiroshi Tsukamoto, Takahiko Horiuchi, Y. Ueda, Yoshiyuki Niho, Kohei Nagasawa, and Kei Ikeda

Subjects
Umbilical Veins, Necrosis, Vascular smooth muscle, Immunology, Enzyme-Linked Immunosorbent Assay, Biology, Complement Hemolytic Activity Assay, Polymerase Chain Reaction, Muscle, Smooth, Vascular, Cell Line, Interferon-gamma, chemistry.chemical_compound, medicine.artery, medicine, Humans, Immunology and Allergy, RNA, Messenger, Northern blot, Aorta, Gel electrophoresis, Tumor Necrosis Factor-alpha, Complement C4, Muscle, Smooth, Complement C3, Molecular biology, chemistry, Cell culture, Phorbol, Electrophoresis, Polyacrylamide Gel, medicine.symptom, Research Article
Abstract

Production of the third and fourth components of complement (C3, C4) by smooth muscle cells was investigated by using normal human aortic smooth muscle cells (AoSMC), human smooth muscle cell line (G402) and vascular smooth muscle cells obtained from human umbilical cord vein (UVSMC). AoSMC spontaneously produced both C3 and C4 at 15 ng/10(6) cells/72 hr and 22 ng/10(6) cells/72 hr, respectively, and both were enhanced by interferon-gamma (IFN-gamma). Although phorbol 12-myristate 13-acetate (PMA) and tumour necrosis factor-alpha (TNF-alpha) enhanced C3 production, C4 production was reduced by these agents. On the other hand, G402 produced C4 but not C3 in a dose-dependent manner when cultured with IFN-gamma. UVSMC produced only a small amount of C3 and C4 compared with AoSMC or G402. C3 and C4 produced by AoSMC were confirmed to be identical with their human serum counterparts as determined by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and measurement of haemolytic activity. Northern blotting analysis showed that the expression of mRNA of C3 and C4 was enhanced by TNF-alpha and IFN-gamma, respectively, in AoSMC. Our findings suggest the importance of smooth muscle cells as a source of components of complement in vascular diseases including vasculitis.

Published
1996

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