Publication: Impairment of CD4CD25+ regulatory T cells in C4-deficient mice
Issued Date
2011-09-27
Resource Type
ISSN
22288694
0125877X
0125877X
Other identifier(s)
2-s2.0-80053070362
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Mahidol University
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SCOPUS
Bibliographic Citation
Asian Pacific Journal of Allergy and Immunology. Vol.29, No.3 (2011), 220-228
Suggested Citation
Pornsawan Leaungwutiwong, Wannaporn Ittiprasert, Kulnasan Saikhun, Pirut Tong-Ngam, Siriwat Akapirat, Siriporn Chattanadee, Yindee Kitiyanant Impairment of CD4CD25+ regulatory T cells in C4-deficient mice. Asian Pacific Journal of Allergy and Immunology. Vol.29, No.3 (2011), 220-228. Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/11989
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Title
Impairment of CD4CD25+ regulatory T cells in C4-deficient mice
Abstract
Objective: To investigate the association between deficiencies of early components in the classical complement pathway and the development of SLE. Methods: Forty inbred C57BL/6J mice and 40 knockout C4 complement gene (C4KO) mice, which included 10 mice in each age group (2, 4, 6, and 8 months) were used. The enumeration of CD4+CD25+ Tregs frequencies in bone marrow, spleen and peripheral blood from both normal and C4KO groups were performed by flow cytometry. The expression levels of Foxp3 and TGF-β in the same tested tissues were measured using real time PCR. The antinuclear antibodies (ANA) were semi-quantitatively measured using ELISA. Results: We report decreased frequencies of CD4+CD25+ Tregs and reduced expression levels of Foxp3 and TGF-β, which efficiently program the development and function of Tregs, in lymphoid tissues and peripheral blood of C4KO mice. In this study, C4KO mice have higher titers of ANA than those of normal mice. Higher frequencies of mice positive for ANA are also found in older mice. Conclusions: The deficiency of the C4 gene induces the decreased numbers of Tregs that further increase the production of ANA resulting in the development of an autoimmune disorder. The outcomes of our study help us to understand the association between the deficiency of C4 in the classical complement pathway and development of autoimmune disorder via the role of Tregs.