In late-stage multiple sclerosis, inflammatory cells no longer enter the brain via the bloodstream, but instead the cells arise in memory from local memory cells inside the brain. The findings suggest during the late phases of multiple sclerosis, the disease is occurring entirely inside the brain.
Introducing VEGF-C into the cerebrospinal fluid of mouse models of glioblastoma, researchers noted increased levels of T cell response to the cancerous tumors. When combined with immune system checkpoint inhibitors, the VEGF-C treatment significantly extended the life span of the mice with glioblastoma brain cancer.
The fetal gut has far better developed immune capabilities than previously thought. The findings could help develop new maternal vaccines and provide early insight into potential autoimmune disorders, which may occur later in life.
Injecting extracellular vesicles from healthy mice into mice that had an MS-like disease resulted in the development of a relapse-remitting disease and active CD8+ cells, similar to that seen in human patients with multiple sclerosis. Examining the EVs in mice and humans with MS, researchers identified they contained fibrinogen, a protein normally associated with blood clotting and wound healing. According to researchers, the EVs with fibrinogen appear to activate the CD8+ immune cells. The findings could help with the development of new treatments for RRMS.
Researchers say in some autoimmune disorders, such as Rasmussen's encephalitis, neurons are not only the targets for immune system attacks, but may also be active protagonists.
Researchers report the cytomegalovirus may actually boost, not weaken, our immune systems.
Researchers report TOX, a DNA binding factor, may play a significant role in triggering multiple sclerosis. The study reports TOX promotes T cells to initiate autoimmune tissue destruction in the brain.
Johns Hopkins researchers utilize AI technology to create a map which compares different cellular receptors on the surface of T-cells.