In this study, we found that the average copy number variation (CNVA) of chromosome fragments was a good indicator of immune infiltration and immunotherapy efficacy. Furthermore, CNVA was closely correlated with tumor mutational burden (TMB) and may become a substitute for TMB.

Patients with multiple myeloma (MM) are at increased risk for infection, and clinical assessment of infection risk is increasingly challenging in the era of immune-based therapy. A pilot systems-level immune analysis identified gene expression immune signatures that may predict future infection risk in patients with relapsed and/or refractory MM.

Deleterious mutations in DOCK8 cause a severe immune deficiency syndrome, but whether thymic self-tolerance mechanisms are affected has been unclear. In this study, we found that DOCK8-deficient mice have normal clonal deletion of self-reactive T cells at two stages of development in the thymus. However, DOCK8 deficiency conferred a T-cell-intrinsic defect in the intrathymic differentiation of Foxp3⁺ T-regulatory cells.

Nalfurafine enabled recovery and remyelination during chronic experimental autoimmune encephalomyelitis by targeting the kappa opioid receptor. Furthermore, nalfurafine reduced immune cell infiltration into the central nervous system, altered peripheral immune responses, and enabled remyelination after chronic non-immune demyelination. Our findings support the potential of nalfurafine to promote recovery and remyelination and highlight its promise for clinical use in multiple sclerosis.

In this review, we provide a summary of the current literature profiling intrinsic and extrinsic mechanisms of NK cells that promote dysfunctional responses in solid tumor microenvironments. We critically analyse the current literature and propose open questions as well as new directions for NK-cell-based immunotherapies in cancer.

Therapeutic vaccination exploiting the antigen presentation capacity of dendritic cells to prime and/or boost HBV-specific T-cell responses was deemed highly promising but has not yet delivered its promise. In this review, we summarize what has been clinically tested in terms of antigen targets and vaccine forms, how the immunological and therapeutic effects were assessed and what clinical and immunological findings were reported. We combine this information with the most recent insights on HBV antigen presentation, T-cell responses, vaccine composition, antiviral and immune-modulatory drugs and disease biomarkers to derive novel opportunities for the next generation of therapeutic vaccines.

Specialised diets that produce high concentrations of acetate are a novel approach to protect against intestinal bacterial infections. We show that modified starches yielding short-chain fatty acids delivered during gut infection mediate functional microbiota changes and intraepithelial lymphocyte expansion and activation via GPR43 central to aid in preserving epithelial barrier integrity and bacterial clearance.

Natural killer (NK) cells integrate signals from both innate and adaptive immune components to act as regulatory and effector cells in the immune response to pathogens. Here, we review how distinct viruses, malaria parasites and emerging infections interact with NK cells and influence the differentiation of NK cells and the consequences for their phenotypic and functional characteristics.

The actual immunological correlate(s) of protection from tularaemia in humans remain(s) unknown. As with smallpox, take is widely accepted as a clinical correlate of protection against tularaemia. We report, for the first time, a correlation between take-lesion size and cellular-mediated immune responses in humans after tularaemia immunization.

In this study, we demonstrated that rheumatoid arthritis CD14⁺ monocytes are metabolically re-programmed for sustained induction of pro-inflammatory responses, an effect that is mediated by STAT3 signalling and precedes clinical disease onset.

We observed an age-associated decline of lung-resident memory CD8⁺ T cells in the elderly. The loss of the resident memory T-cell pool that occurs with advanced age coincided with an impairment in the early antiviral immune response following exposure to influenza virus and SARS-CoV-2, a phenomenon that may, in part, explain the increased vulnerability of the elderly to respiratory infections.