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Among the multi-organ complications of Long COVID, those associated with cardiometabolic syndrome were some of the most prevalent in recent studies of population-scale data. Given the potential health and economic burdens, there is an urgent need to better define the inflammatory processes involved.
Human immunology may soon benefit from the use of artificial intelligence and blockchain technologies. Here, we discuss how Swarm Learning could foster collaborative worldwide immunology studies that fully respect local data privacy regulations by sharing insights, not data.
In individuals with Down syndrome, immune dysregulation is partially caused by chromosome 21 trisomy. Here, we discuss how these immune differences may result in poorer COVID-19 outcomes, including diminished responses to vaccination and possibly elevated risk for long COVID.
FlipFlop mice, in which the coreceptor proteins encoded by the Cd4 and Cd8 loci are reversed, shed light on the importance of T cell receptor signal length versus signal strength in determining helper versus cytotoxic T cell lineage fates.
Lymph node colonization by tumour cells promotes subsequent spread to distant tissues by inducing broad alterations in tumour immunity and generating tumour-specific immune tolerance.
The amino acid leucine promotes an immunosuppressive population of B cells, and dietary restriction of leucine could benefit patients with colorectal cancer.
A preprint by Ho et al. investigates the role of decreased CD58 expression in cancer cell immune evasion, through both lack of T cell co-stimulation and increased T cell inhibition.
The renin–angiotensin, complement and kallikrein–kinin systems comprise a multitude of mediators that modulate physiological responses during inflammatory and infectious diseases. This Review investigates the complex interactions between these systems and how these are dysregulated in various conditions, including cardiovascular diseases and COVID-19, as well as their therapeutic implications.
Non-alcoholic steatohepatitis (NASH) is a serious chronic liver disorder of increasing prevalence worldwide. Metabolic by nature, the disease also mobilizes the immune system. Here, Huby and Gautier discuss current knowledge regarding how diverse immune cell subsets affect NASH onset and progression.
In this Review, Manabe and Heneka examine how the systemic inflammation associated with sepsis can lead to acute cerebral dysfunction known as sepsis-associated encephalopathy (SAE). Moreover, they suggest that some of the mechanisms involved in SAE may be relevant for understanding the cognitive impairments that develop in some patients with COVID-19.
