T cell senescence and its correlation to inflammaging process of patients with systemic lupus erythematosus

• Published in: AIP conference proceedings Vol. 2108; no. 1
• Main Authors: Ulfah, Fahrina, Octaviani, Hanani, Handono, Kusworini, Kalim, Handono
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Melville American Institute of Physics 04.06.2019
• Subjects: Aging (natural); Chronic conditions; Correlation analysis; Cytokines; Lymphocytes; Pathogenesis; Senescence
• ISSN: 0094-243X; 1551-7616
• DOI: 10.1063/1.5110006

SLE patients suffered from morbidities resembled the natural aging process, suggesting chronic inflammation in SLE is correlated to premature immune senescence. However, understanding of immune senescence in SLE is not well established. The purpose of this study was to investigate the association of CD4+ and CD8+ T cells senescence markers of end differentiated T cell (CD28-), memory T cell (CD45RO+) and cytokines correlated to inflammaging (IL-2, and IFN-γ) among 61 SLE subjects aged 16-56 years. We measured the percentages of T cell senescence by flow cytometric analysis. Serum IL-2 and IFN-γ were measured by ELISA. Among 61 subjects, percentages of SLE subjects with increased senescence cells ranges from 3.2-58.3%. There was a positive correlation between the percentage of senescent T cells and serum IFN-γ (CD4+CD45RO+; p = 0.003, r = 0.453; CD8+CD45RO+; p = 0.045, r = 0.284; and CD4+CD28-; p = 0.029, r = 0.257) and negative correlation for the percentage of senescent T cells and serum IL-2 (CD4+CD28-; p = 0.014, r = −0384; CD8+CD28-; p = 0.012, r = −0394; CD4+CD45RO+; p = 0.023, r = −0.322; and CD8+CD45RO+; p = 0.017, r = −0.335). This study confirms the role of immune senescence in SLE pathogenesis, particularly in regard to the observed loss of CD28 and increased percentages of CD45RO expression from both CD8+ and CD4+ T cells. We also found the inflammaging process in SLE was correlated to T cell senescence. Studies of immune senescence might provide new opportunities for better understanding of SLE pathogenesis.