Particulate Matter and Its Components Induce Alteration on the T-Cell Response: A Population Biomarker Study

Abstract

Compared with the T-cell potential of particulate matter (PM) in animal studies, comprehensive evaluation on the impairments of T-cell response and exposure−response from PM and its components in human population is limited. There were 768 participants in this study. We measured environmental PM and its polycyclic aromatic hydrocarbons (PAHs) and metals and urinary metabolite levels of PAHs and metals among population. T lymphocyte and its subpopulation (CD4 + T cells and CD8 + T cells) and the expressions of T-bet, GATA3, RORγt, and FoxP3 were measured. We explored the exposure−response of PM compositions by principal component analysis and mode of action by mediation analysis. There was a significant decreasing trend for T lymphocytes and the levels of T-bet and GATA3 with increased PM levels. Generally, there was a negative correlation between PM, urinary 1-hydroxypyrene, urinary metals, and the levels of T-bet and GATA3 expression. Additionally, CD4 + T lymphocytes were found to mediate the associations of PM 2.5 with T-bet expression. PM and its bound PAHs and metals could induce immune impairments by altering the T lymphocytes and genes of T-bet and GATA3.

Crystalline silica-induced recruitment and immuno-imbalance of CD4 + Tissue Resident Memory T cells promote the progression of silicosis.

“…The inhaled CS particles deposited in the lung interstitium trigger inflammatory cascades involving innate and adaptive immune responses [6] . Although some early events, such as macrophages response to CS particles, in silicosis are clear, the following steps leading to fibrosis are less well-understood [7,8,9] . Different from the simple exposure-response relationship, adaptive immune response characterized as disorders of T lymphocytes orchestrate chronic inflammation and fibrogenesis [10] .…”