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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. [ABSTRACT FROM AUTHOR]

We developed an animal model for chronic observation with using two-photon microscopy. To demonstrate potency of the model, T-cell migration and proliferation in inguinal lymph node were observed for two weeks on single mice. The image quality was maintained enough high during a observation period to count and trace cell population and migration. [ABSTRACT FROM PUBLISHER]

The research of immune cells is fundamental to many biological studies. Dendritic cells have the ability to induce a primary immune response in resting naive T cells. The aim of this work is to separate the activated T cells from dendritic cells on a digital microfluidic device where droplets are driven by electrowetting-on-dielectric (EWOD). The cells suspended in EWOD-driven droplets are separated and concentrated using a high frequency electric signal which generates non-uniform electric fields and dielectrophoresis (DEP) forces exerting on dendritic cells and T cells. Separation and concentration of dendritic cells and T cells are demonstrated in a droplet using EWOD and DEP. [ABSTRACT FROM PUBLISHER]

Mesenchymal stem cells (MSCs) have been thought to be a potential mode of therapy for immuno-related pathologies, particularly autoimmune diseases. Specifically, the ability to impart immunomodulatory effects on target inflammatory sites makes the use of MSCs particularly attractive for patients affected by taking immunosuppressive medicine, which works to downregulate the immune system on a systemic level. Despite its promises, the interaction between MSCs and T-cells, a key player in the pathophysiology of autoimmune diseases, is not yet well understood, thereby preventing further progress in the clinic. A major obstacle is the highly heterogeneous nature of MSCs in-vitro. Bulk assays commonly carried out discount the inherent heterogeneity, and thus do not provide information with regards to single-cell contributions that may play a critical role in the overall bulk response. To address these issues, we propose to study the single-cell interaction between MSCs and CD4 T cells in a nanowell array. Using the nanowell assay, we demonstrate that individual MSCs appear capable of dynamically modulating the T cell proliferation rate in response to persistent cell-cell interactions in a microenviroment. Based on these results, we anticipate the use of our nanowell assay in the classification of subpopulations within MSCs, ultimately leading to specific therapeutic interventions. [ABSTRACT FROM PUBLISHER]