Early-stage detection of colorectal cancer is critical for patient survival. We have conducted a multi-isotype autoantibody (AAbs) screen using a 492-feature CRC protein array. Our study shows that IgM AAbs are associated with early-stage disease and IgA AAbs, although stage-independent, encompass humoral responses associated with mucosal surfaces. Combining IgG, IgM and IgA AAbs is a novel strategy for early disease detection and improvement of patient outcomes.

This study defines two distinct subsets of effector regulatory T cells (Treg) circulating in the human blood based on the presence or absence of CD49f with divergent transcriptional landscape and functional activities. CD49f^– Treg are enriched for functional Treg markers and present significantly increased suppressive capacity whilst CD49f^high Treg display a pro-inflammatory Th17-like phenotype and accumulate in patients with ulcerative colitis (UC). Dysregulation of CD49f Treg subsets in patients with UC correlates with disease activity and may be assessed as a way to improve UC immune monitoring.

In this study, we report on the potential of a modular multi-pathogen mucosal vaccine. We found that this vaccine construct induces an Immunoglobulin A (IgA) response in both mice and ferrets. Vaccination reduces viral load in ferrets from influenza challenge and protects mice from influenza virus:S. pyogenes super-infection.

In this study, we found that supranutritional selenium (Se) was associated with improved disease activities in patients with rheumatoid arthritis and also ameliorated collagen-induced arthritis in mice. Se attenuated the production of reactive oxygen species (ROS) and thus suppressed ROS-mediated induction of RANKL expression in activated CD4⁺ T cells.

We longitudinally studied moderate-to-severe COVID-19 patients to dissect SARS-CoV-2-specific B cell responses overtime. We found a broad virus-specific antibody response during acute infection, which evolved into an IgG1-dominated response. Moreover, we identified a persistent expansion of virus-targeting naïve-like and memory B cells in COVID-19 patients, as well as unique immune signatures that associated with disease severity and inflammation.

Simnica et al. report on public T-cell receptors in immune responses to SARS-CoV-2, which are shared between patients and non-exposed individuals. Their lower prevalence in older age and cancer could imply why these risk groups may experience more severe COVID-19 courses.

Low-affinity antigens triggering weak TCR signalling (Signal 1) require CD28 costimulation (signal 2) to elicit T-cell responses. In this study, we found that miR-21 sustains the CD28 costimulation pathway, via inhibition of its repressors in a positive feedback circuit, decreasing the T-cell activation threshold. This broadens the range of detected antigens, at the cost of unleashing autoimmunity resulting from the recognition of weak self-antigens by autoreactive T cells. Thus, miR-21 fine-tunes T-cell response and self/non-self-discrimination.

In this study, we demonstrated quantitative and functional disruptions in the regulatory immune response of patients with giant cell arteritis, resulting in increased proliferation and Th17 polarization of effector T cells. In addition, our results suggest that, through a specific blockade of the IL-6 pathway, tocilizumab associated with glucocorticoids restores a better quantitative and qualitative Treg immune response than glucocorticoids alone. GCA, giant cell arteritis. Teff, effector T-cells; Th17, T helper-17 cells; Treg, regulatory T-cells.

Severe H7N9 infection in mice induces CD38⁺MHC-II⁺PD-1⁺ activation profiles. These data reflect findings from H7N9-hospitalised patients with severe and fatal disease outcomes.

In this study, we found that a single dose of BNT162b2 vaccine generates a strong humoral (100%) and cellular response in convalescent COVID-19 individuals (94%), and also in infection-naïve healthcare workers with cross-reactive immunity because of other coronaviruses (93%). However, this response was not observed in convalescent individuals with previous loss of specific antibodies after the disease, who had a T-cell response similar to that of other infection-naïve individuals. Thus, different factors could influence the rate of humoral and cellular responses to the vaccine.

This review summarises the current evidence of the acute and long-term cardiovascular consequences of SARS-CoV-2 infection and the mechanisms by which SARS-CoV-2 may cause cardiovascular disease.