The atmospheric particulate matter with a diameter less than or equal to 2.5 um (PM2.5) can result in increased immune system damage or diseases, however, the possible mechanism remains unclear. In this study, we used Jurkat T cells to determine the effects of PM2.5 on T cell-mediated adaptive immune response. Our results indicated that PM2.5 exposure increased intracellular calcium ion concentration [Ca(2+)]. In contrast, cytosolic free Ca(2+) concentration [Ca(2+)]i significantly decreased in Jurkat T cells transfected with Orai1siRNA. In addition, we detected the level of interleukin (IL)-2 and tumor-necrosis factor (TNF)-α as well as other signalling molecules, including calcineurin (CaN) and NFATc2, a gene on 20q13.2 that encodes a member of the nuclear factor of activated T cells (NFAT), in the supernatant of cells exposed to PM2.5. The expression of NFATc2 protein increased in a time-dependent manner after exposure to PM2.5, but the activity of CaN decreased. NFATc2 was not consistent with IL-2 accumulation, thus indicating the involvement of other signals in the suppression of IL-2 accumulation. Our findings demonstrate that PM2.5 exposure in immune cells results in locally increased [Ca(2+)]i generated by Orai1 and CaN-NFAT gene expression, TNF-α and IL-2 cytoplasmic concentrations may be altered.

Traffic-related PM 2.5 can result in immune system damage and diseases; however, the possible mechanism of its effect remains unclear. Calcium (Ca 2þ) is a critical signaling molecule in a variety of cells. Indeed, Ca 2þ is involved in numerous basic functions, including cell growth and death. In this study, Jurkat T cells were used to explore the possible mechanisms of PM 2.5-elicited intracellular Ca 2þ signal responses. The results indicate that PM 2.5 could raise the level of intracellular Ca 2þ concentration ([Ca 2þ ]i). The [Ca 2þ ]i in Jurkat T cells significantly decreased after treatment with heparin as an inhibitor of inositol trisphosphate receptors (IP3 R), or procaine as an inhibitor of ryanodine receptors (RyR). The expression of calmodulin (CAM) protein decreased in a time-dependent manner after exposure to PM 2.5 , whereas the activity of Ca 2þ-Mg 2þ-ATPase seemed to show a slight drop trend after exposure to PM 2.5. Our findings demonstrate that PM 2.5 stimulation to Jurkat T cells would result in an increase in [Ca 2þ ]i, which is modulated by IP3 R and RyR, as well as CAM.

Follicular CXCR5 + CD8 + T cells have antiviral effects in chronic virus infection, but the roles of these cells during dengue virus 2 (DENV2) infection remain poorly understood. Objective: This study was conducted to analyzed in detail the dynamic changes and functional properties of circulating follicular CXCR5 + CD8 + T cells to explore their effects on DENV2 infection. Methods: Circulating follicular CXCR5 + CD8 + T cells and cytokines were analyzed by flow cytometry in DENV2 patients at difference days after DENV2 infection. CD8 + T cells were isolated and purified from DENV2 patients, then were stimulated with NS1 peptides and TCR stimulant. After cultivation, multiple parameters were tested. Results: (1) CXCR5 + CD8 + T cells emerged after DENV2 infection, with high PD-1 expression, and were correlated with the reduction in DENV2 RNA viral loads. (2) PD-1 + CXCR5 + CD8 + T cells were negatively associated with disease progression. (3) Serum IFN-g, IL-6 and IL-10 levels were increased late in the course of DENV2 infection. (4) CXCR5 + CD8 + T cells from DENV2 patients exhibited increased cytotoxicity and IFN-g and IL-10 secretion. Conclusion: CXCR5 + CD8 + T cells could play a protective role in dengue pathogenesis and may be a novel strategy for controlling DENV2 infection and vaccine development.

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Dengue fever, a highly infectious disease transmitted by Aedes mosquitoes, is caused by four serotypes of dengue virus (DENV), which has led to 400 million infections annually in over 100 countries. 1 Most infections are subclinical; however, in some cases, DENV infection results in a variety of clinical symptoms, ranging from mild fever (dengue fever) to dengue shock syndrome and dengue hemorrhagic fever, which is fatal. 2,3 Currently, no approved antiviral drugs are available to treat DENV infection; therefore, the only management option for patients is symptomatic treatment. 4,5 DENV infection induces the expansion of memory B cells and plasmablasts. [6][7][8][9][10] Plasmablasts further differentiate into antibodysecreting plasma cells associated with an antigen-specific B-cell