Myeloid cell-like transcript 2 is related to liver inflammation and the pathogenesis of hepatitis B via the involvement of CD8⁺T cell activation.

This study analysed the biological significance of TLT-2 on CD8⁺T cells in hepatitis B patients and provided a theoretical basis for the potential role of TLT-2 as an immune regulator. Flow cytometry sorting, isobaric tags for relative and absolute quantitation and short hairpin RNAs were used to analyse the function of TLT-2 on CD8⁺T cells in hepatitis B patients. The TLT-2 expression levels in the acute hepatitis B and chronic hepatitis B groups were significantly higher than that in the healthy control group and were positively correlated with ALT and AST. The CD8⁺TLT-2⁺T cells exhibited stronger immune function and greater cell proliferation ability and secreted higher levels of cytokines than the CD8⁺TLT-2^-T cells. An analysis of the proteome differences between the TLT-2⁺CD8⁺T and TLT-2^-CD8⁺T cells revealed that TLT-2 affected CD8⁺T cell activation by regulating Granzyme B expression and by further action on the NF-κB signalling pathway. This study first elucidated the mechanism by which TLT-2 influences the activation of CD8⁺T cells, improved the understanding of the TLT-2 signalling pathway and clarified the role of the TLT-2⁺CD8⁺T cell subset in hepatitis B virus infection. The study proposed a novel subset of CD8⁺T cells that could be useful for understanding the immune function of patients with hepatitis B and further elucidating the pathogenesis of hepatitis B by analysing changes in this subpopulation with the goal of providing a new target for the treatment of hepatitis B.

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