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. 2018 May 17;42(2):703–712. doi: 10.3892/ijmm.2018.3688

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Copyright: © Cao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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CD4⁺ Th cells have similar susceptibility to apoptosis to CD8⁺ T cells following persistent HBV infection. Upregulated expression of CTLA-4 on CD4⁺ Th cells polarizes them toward the Th2 and iTreg phenotypes, which results in an increase of anti-inflammatory cytokine (TGF-β, IL-10, and IL-4) levels. Conversely, the differentiation of proinflammatory cells, such as Th1, TFH and CD4⁺ Th cells, is blocked, and the levels of proinflammatory cytokines (IL-2, IL-21, and IFN-γ) is decreased. Th, T helper cells; HBV, hepatitis B virus; CTLA-4, cytotoxic T lymphocyte-associated antigen-4; iTreg, peripherally-inducible Treg; TGF, transforming growth factor; IL, interleukin; TFH, follicular helper T cells; IFN, interferon.