#t-cell-proximity

#t-cell-proximity

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.

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.

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.

Tumours lure and then hijack nearby sensory neurons to boost their own growth. The cancer cells use these neurons to send a signal to the brain that subdues the activity of immune cells around the tumour, which allows it to grow unchecked. When researchers deactivated these neurons in mice with lung cancer, they saw "a huge, dramatic reduction" in tumour growth - more than 50% - says cancer immunologist and study co-author Chengcheng Jin.

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.