Viral sequence determines HLA-E-restricted T cell recognition of hepatitis B surface antigen.

Murugesan, Gavuthami; Paterson, Rachel L; Kulkarni, Rakesh; Ilkow, Veronica; Suckling, Richard J; Connolly, Mary M; Karuppiah, Vijaykumar; Pengelly, Robert et al. · Nat Commun · 2024

basic_science · Level V

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Abstract

The non-polymorphic HLA-E molecule offers opportunities for new universal immunotherapeutic approaches to chronic infectious diseases. Chronic Hepatitis B virus (HBV) infection is driven in part by T cell dysfunction due to elevated levels of the HBV envelope (Env) protein hepatitis B surface antigen (HBsAg). Here we report the characterization of three genotypic variants of an HLA-E-binding HBsAg peptide, Env<sub>371-379,</sub> identified through bioinformatic predictions and verified by biochemical and cellular assays. Using a soluble affinity-enhanced T cell receptor (TCR) (a09b08)-anti-CD3 bispecific molecule to probe HLA-E presentation of the Env<sub>371-379</sub> peptides, we demonstrate that only the most stable Env<sub>371-379</sub> variant, L6I, elicits functional responses to a09b08-anti-CD3-redirected polyclonal T cells co-cultured with targets expressing endogenous HBsAg. Furthermore, HLA-E-Env<sub>371-379</sub> L6I-specific CD8<sup>+</sup> T cells are detectable in HBV-naïve donors and people with chronic HBV after in vitro priming. In conclusion, we provide evidence for HLA-E-mediated HBV Env peptide presentation, and highlight the effect of viral mutations on the stability and targetability of pHLA-E molecules.

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