#dendritic-cells

#dendritic-cells

Chronic inflammation is a central driver of pathological fibrosis after ischaemic or haemodynamic stress, but strategies that locally rebalance injurious and reparative immune responses without systemic immunosuppression are lacking.

The thymus is a specialized immune organ responsible for maturing T cells, thereby producing a diverse T cell repertoire crucial for mounting an adaptive immune response. The thymus itself decays with age and eventually transforms entirely into adipose tissue through a process known as thymic involution.

During viral infection and in the case of cancer, CD4+ helper T-cells release cytokines, or small signaling proteins, that activate and "give permission" to other immune cells to control and clear viral pathogens. In certain viral infections, such as lymphocytic choriomeningitis virus (LCMV), which is spread by infected rodents, CD4+ T-cells differentiate into different subpopulations, including one subset of progenitor CD4+ T-cells that replenish type 1 helper (Th1) and follicular helper (Tfh) T-cells.

Ferroptosis, a major mechanism of non-apoptotic programmed cell death, critically regulates the homeostasis and functionality of peripheral CD4+ and CD8+ T cells. Here we demonstrate that in mouse, resistance of T cells to ferroptosis depends critically on the composition of standard rodent diets, and that dietary effects on ferroptosis have a crucial role in regulation of T cell homeostasis and immune responses.

Although specific bacterial taxa have been associated with favourable clinical responses to immune checkpoint blockade (ICB) in cancer patients12,13,18,19,20,21,22, the mechanisms by which the intestinal microbiota influences anti-tumour immune responses remain poorly defined. Products of the microbiota, including metabolites23,24,25 and innate receptor ligands26, may reprogramme myeloid cells27, lowering the activation threshold for antigen presentation and thereby facilitating priming and activation of tumour-reactive T cells.

For years, scientists have viewed cancer as a localized glitch in which cells refuse to stop dividing. But a new study suggests that, in certain organs, tumors actively communicate with the brain to trick it into protecting them. Scientists have long known that nerves grow into some tumors and that tumors containing lots of nerves usually lead to a worse prognosis.

Exposure to cytosolic DNA triggers innate immune responses through cyclic GMP-AMP (cGAMP) synthase (cGAS)1,2,3. After binding to DNA, cGAS produces cGAMP as a second messenger that binds to stimulator of interferon genes (STING), a signalling adaptor protein anchored to the endoplasmic reticulum (ER)3,4,5. STING then traffics from the ER through the Golgi to perinuclear vesicle clusters, which leads to activation of the kinases TBK1 and IKK and subsequent induction of interferons and other cytokines6,7,8,9.