Publications by authors named "Chanidapa A Tye"
Article Synopsis
- T cell pathology in the skin causes an influx of monocytes, but we lack knowledge about how these recruited cells behave over time and affect immune balance in the skin.
- Research combining a mouse model of acute graft-versus-host disease (aGVHD) and patient samples reveals that disease leads to the differentiation of macrophages specifically in the skin's dermis and results in a dominance of these macrophages, reducing the presence of resting MHCII cells.
- After the disease resolves, exposing the altered skin to certain substances can cause overactivation of regulatory T cells (Tregs), leading to a loss of immune tolerance and an enduring impact on immune regulation, referred to as an "immunological scar."
T-cells play key roles in immunity to COVID-19 as well as the development of severe disease. T-cell immunity to COVID-19 is mediated through differentiated CD4 T-cells and cytotoxic CD8 T-cells, although their differentiation is often atypical and ambiguous in COVID-19 and single cell dynamics of key genes need to be characterized. Notably, T-cells are dysregulated in severe COVID-19 patients, although their molecular features are still yet to be fully revealed.
View Article and Find Full Text PDFSevere COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19.
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