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The percentages of cells with depolarized mitochondria are shown below the dashed line.(B)Mean percentage (and SD) of lymphocytes with depolarized mitochondria obtained from independent experiments performed in cells from 15 healthy donors is also shown. (from 0.15 to 60 g/ml) and at different time points (from 24 h to 9 days) of either E4 or E5 particles. Immunological parameters, including apoptosis, autophagy, proliferation levels, mitochondrial function, expression of activation markers and cytokine production were evaluated by cellular and molecular analyses. == Results == DEP exposure caused a pronounced autophagic-lysosomal blockade, thus interfering with a key mechanism involved in the maintaining of T cell homeostasis. Moreover, DEP decreased mitochondrial membrane potential but, unexpectedly, this effect did not result in changes of the apoptosis and/or necrosis levels, as well as of intracellular content of adenosine triphosphate (ATP). Finally, a down-regulation of the expression of the alpha chain of the interleukin (IL)-2 receptor (i.e., the CD25 molecule) as well as an abnormal Th1 cytokine expression profile (i.e., a decrease of IL-2 and interferon (IFN)- production) were observed after DEP exposure. No differences between the two compounds were detected in all studied parameters. == Conclusions == Overall, our data identify functional and phenotypic T lymphocyte parameters as relevant targets for DEP cytotoxicity, whose impairment could be detrimental, at least in the long run, for human health, favouring the development or the progression of diseases such as autoimmunity and cancer. == Electronic supplementary material == The online version of this article (doi:10.1186/s12989-014-0074-0) contains supplementary material, which is available to authorized users. Keywords:Air pollution, DEP, T lymphocytes, Autophagy, Mitochondria, IL-2 == AN3199 Background == Particulate matter in air pollution is associated with adverse health effects such as asthma and cardiovascular diseases as well as lung cancer mortality [1-4]. Diesel exhaust particles (DEP) emitted by diesel engines consist of fine particles (particulate matter with an aerodynamic diameter 2.5 m) including a high number of ultrafine particles (< 0.1 m diameter). They are composed of a center core of elemental carbon (80%) and adsorbed organic compounds, including polycyclic aromatic hydrocarbons Odz3 (PAH) and nitro-PAH, and small amounts AN3199 of sulfate, nitrate, metals, and other trace elements. AN3199 All these compounds are considered to be of great toxicological importance. The small size of DEP makes them highly respirable, thus having the potential to reach the deep lung and to translocate to the bloodstream although this latter still remains a debated issue [2,5-10]. In particular, it has been suggested that ultrafine carbon particles, after deposition in the lung, largely escape alveolar macrophage surveillance and gain access to the pulmonary interstitium. From this site, a further translocation of the ultrafine particles to the blood circulation via lymphatic channels or directly via the endothelium could take place [8,9]. A series of studiesin vivorevealed that DEP exposure has remarkable effects on the immune system: pre- and postnatal animal exposures to DEP decrease the weight of the thymus and spleen, accelerate the production of IgE against pollen, increase allergic susceptibility, alter inflammatory indices in the lung, and increase airway hyperesponsiveness [11,12]. These findings in animal models have been partially confirmed inin vitroandin vivohuman studies, and the largest literature in this regard has looked at the link between DEP exposure and allergic diseases. In fact, it has been demonstrated that DEP exposure can both exacerbate existing allergic diseases and cause allergic sensitization by promoting a Th2 cytokine profile [12-24]. The precise mechanism by which DEP exposure promotes allergic responses is not entirely clear, although oxidant activity of the adsorbed PAH, rather than properties specific to the carbon core, appears to be involved. With the exception of these studies regarding cytokine production, scant data are available on the impact of DEP on lymphocyte phenotype and function. This topic has substantial importance in light of evidence that aberrant lymphocyte homeostasis can result in several diseases including autoimmune, allergic and even neoplastic diseases. In one study, chronicin vitroexposure of T lymphocytes to DEP-PHA increased T cell activation marker expression and proliferation in asthmatics but not in controls AN3199 [19]. More recently, Vattanasitet al.[25] demonstrated that reactive oxygen species generation and oxidative DNA damage were induced by DEP in both lymphoblasts and lung cells suggesting that lymphocytes could be used as a surrogate to assess DEP-dependent responses in the lung. No data are currently available on the effects of DEP on T cell fate in terms of apoptosis or autophagy. This latter is a lysosome-mediated catabolic process that allows cells to degrade unwanted cytoplasmic constituents and recycle nutrients [26], and it has been recently emerged as a key parameter, in addition to apoptosis [27],.