CD8-positive T cells articles from across Nature Portfolio

Here the authors show how the liver affects the immune response to pancreatic ductal adenocarcinoma and that cancer immunity and survival outcomes after surgery might be bolstered by therapeutic intervention on hepatocyte release of serum amyloid A proteins.

Interactions between Semaphorin-3A (SEMA3A) and Neuropilin-1 (NRP1) and Plexin-A1 and Plexin-A4 have been shown to affect T cell development. Here the authors investigate how these interactions affect CD8⁺ T cells in tumour immunity, showing that NRP-1, Plexin-A1 and Plexin-A4 are upregulated on T cells allowing tumour derived SEMA3A to inhibit CD8⁺ T cell migration and function.

The heterogeneity in naive CD8⁺ T cells is essential for diverse immune responses. Here the authors show that variations in developmental self-reactivity of CD8⁺ T cells influence their differentiation into T_c17 cells in inflammatory conditions.

Obesity represents a risk factor for cancer and compromises immune function, however the mechanisms linking the two together are not fully known. Here authors show in a mouse sarcoma model that obesity increases tumour incidence, impairs intra-tumoral T cell immunity but paradoxically increases sensitivity to immune therapy via impairing immunoediting.

The migration of T cells into tumours and how this is regulated by metabolic pathways is not completely understood. Here the authors use human and xenograft mouse models to explore the functional changes in T cells during migration in tumours and how glycolytic and TCA cycle metabolism is involved.

The reasons for why hepatocellular carcinoma (HCC) is unresponsive to anti-PD-1 inhibition in some patients is not fully understood. Here the authors use human samples and mice tumour models to implicate serum amyloid A and STAT3 signalling involvement in the resistance to anti-PD1 immunotherapy in HCC.

The transcription cofactor TLE3 interacts with RUNX3 and TCF1 to repress the transcription and chromatin accessibility of CD8⁺ T_CM cell signature genes, while simultaneously acting as a coactivator for TBET to facilitate the expression of CD8⁺ T_EM cell signature genes. As such, TLE3 serves as a gatekeeper of CD8⁺ T_CM cell formation.

The failure of T cell-targeted vaccines for HIV in clinical trials is likely due to impaired degranulation of low-avidity CD8⁺ T cells in the context of low levels of antigen presentation.