A study from the University Medical Center Hamburg-Eppendorf (UKE) in Germany has identified a type of T cell that triggered glomerulonephritis (GN) and produced loss of kidney function in mice. The scientists described an autoimmune pathway of this disease mediated by the accumulation of T cells producing granulocyte-macrophage colony-stimulating factor (GM-CSF) in the kidneys and found a possible therapeutic target.
T cells do not have the last word in some breast cancers. According to a study from the University of Pittsburgh, the key to estrogen receptor positive (ER+) breast tumors are macrophages, not T cells, and targeting them could prevent immunotherapy failure in this type of cancer.
The traps that neutrophils develop against microorganisms also hold T cells and prevent the success of immunotherapy in pancreatic cancer. To free the immune system from itself, scientists at the Istituto Oncologico Veneto in Italy made a key that unlocked this sticky dungeon from an antibody against arginase-1 (ARG1), an enzyme also present in the trap.
Losing the tail to survive. In neurons, the lizard’s strategy, losing the axon to be safe, could prevent cell death. Scientists at Harvard Medical School have observed that certain toxins activated axon loss to prevent damage and survive. This mechanism was mediated by the Gasdermin-E (GSDME) protein, which destroyed the mitochondria in the axons and eliminated the affected nerve projection before the cell died. The inhibition of GSDME prevented the loss of neurons and delayed the progression of amyotrophic lateral sclerosis (ALS) in mice models.
Two molecules that affected the cell cycle only of acute myeloid leukemia (AML) cells could be used as a clinical strategy against this pathology. Scientists at Memorial Sloan Kettering Cancer Center and Harvard University have discovered that DEG-35 and DEG-77 arrested the cell cycle and promoted cell differentiation and apoptosis in these cells.
A deficiency in fumarate metabolism could be behind a new mechanism of inflammation mediated by mitochondrial DNA and RNA. Two independent and simultaneous studies described how the accumulation of fumarate in the mitochondria released the genetic material of this organelle through vesicles, activating an inflammatory signaling pathway.
Scientists from Washington University in St. Louis have described a role for T cells in the neurodegeneration associated with the tau protein. Tau accumulation in the brain activated microglia. This signal triggered the activation of T cells in other parts of the body, attracting them to the brain. Once there, the interaction of these T cells and microglia produced the neuronal damage seen in Alzheimer’s disease and other tauopathies.
Autoantibodies are typically not good news. But a group of researchers from Bellinzona, Switzerland, have observed that the presence of autoantibodies against chemokines, a special class of cytokines, is associated with mild disease and less risk of developing long COVID. “Our hypothesis was that antibodies to chemokines, if they existed, would also be associated with a negative outcome of the disease. But, what we found, in fact, was the exact opposite of what we were predicting,” Davide Robbiani, director of the Institute for Research in Biomedicine, told BioWorld.
Bacteria inflaming the meninges have developed an immunosuppressive mechanism that contributes to their ability to attack the brain. Researchers found that, by activating pain receptors (nociceptors) to release chemical substances that block an immune cell receptor, Streptococcus pneumoniae and Streptococcus agalactiae deactivated the protective function of macrophages and weakened brain defenses. This, in turn, enabled them to invade the brain.
Scientists at the University of Virginia have discovered an anti-aging mechanism mediated by an enzyme that metabolizes alcohol. Alcohol dehydrogenase, which in Caenorhabditis elegans and yeast replaces the rejuvenating effect of autophagy, would reduce age-associated glycerol levels, also promoting longevity in mice and humans.
