Secreting cytokines and killing tumor cells can be stressful for a T lymphocyte. In short adverse circumstances, these cells adapt to acute stress. If the situation persists, they activate a chronic stress response mechanism. According to a study by the Institute for Biomedical Research (IRB) in Barcelona, the cytoplasmic polyadenylation element-binding protein 4 (CPEB4) mediated this adaptation process.
Restoring levels of the immune modulator mesencephalic astrocyte-derived neurotrophic factor (MANF) in the muscles of aged animals improved their regenerative capacity by promoting repair-associated injury responses, researchers from the University of Lisbon have discovered.
Base editing (BE), a technique that modifies a single nucleotide in living cells, has been successfully tested to resolve the CD3δ mutation in severe combined immunodeficiencies (SCIDs) and produce functional T cells. For now, scientists at the University of California, Los Angeles (UCLA), completed the study on patient stem cells and artificial thymic organoids, shortening the way for future clinical trials.
Pharming Group NV’s stock skyrocketed March 24 on news that the U.S. FDA approved Joenja (leniolisib) to treat activated phosphoinositide 3-kinase delta syndrome (APDS) for those ages 12 and older. The nod, which came a few days ahead of the March 29 PDUFA date, sent shares (NASDAQ:PHAR) up 33%, or $3.69, to end the day at $14.96.
Phase II data that rolled out from Merck KGaA with its Bruton's tyrosine kinase (BTK) inhibitor evobrutinib in relapsed multiple sclerosis (MS) put more eyeballs on the mechanism. It’s already well validated in oncology, but resistance has arisen there, and at least two firms – Beigene Ltd. and Nurix Therapeutics Inc. – are striving for solutions with degrader candidates.
Incyte Corp.’s bid for a once-daily vs. twice-daily version of the Janus kinase inhibitor Jakafi (ruxolitinib) was foiled, at least temporarily, by a complete response letter (CRL) from the U.S. FDA.
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.
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