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Potentiating dendritic cell immunotherapy by interrupting the Semaphorin 4D-induced immune-suppressive barrier

Garg et al. report that blocking the molecule SEMA4D strengthens immune responses against HER2-positive breast cancer. When paired with specialized dendritic cells, this approach boosts anti-tumor immune activity, reduces suppressive cells, and enables clearance of both local and distant tumors. Their findings support a promising and well-tolerated immunotherapy strategy.

Chemokines CXCL9 and CCL2 in Relation to Cerebral White Matter Disease, Cognitive Decline, and DementiaThe Northern Manhattan Study

This large cohort study showed that higher serum CXCL9 was associated with greater burden of white matter disease in the brain, independent of vascular risk factors, renal function, and genetic predisposition, supporting a role for CXCL9 in white matter pathogenesis.


Background and Objectives.

GLP-1 Receptor Agonists and Noncardiometabolic Outcomes: An Umbrella Review of Meta-Analyses

In this umbrella review of 60 meta-analyses of 1751 RCTs, GLP-1 RAs were associated increased GI adverse events (eg, nausea/vomiting); suggested protective associations with respiratory diseases and serious infections require further confirmation.


This meta-analysis evaluates the reported outcomes of glucagon-like peptide-1 (GLP-1) receptor agonists beyond glycemic control, weight management, and cardiorenal protection and assesses the credibility of the evidence.

Prevalence of early-stage type 1 diabetes in young adults: a population-based cohort study

Individual variability in synaptic gene expression and synapse density in induced pluripotent stem cell–derived neurons predicted macro-scale alterations in gray matter volume and gamma-band activity in patients with Schizophrenia.

SIRS2026.


This genetic association study tests whether genetically driven variability in excitatory neurons’ transcriptome and synapse density in patient-derived neurons in vitro explain individual changes in cortical morphology, electrophysiology, and cognitive impairments in vivo.

A stiff defense: Physical rigidity of healthy gum tissue found to shield against chronic periodontal inflammation

Periodontitis is a serious chronic inflammatory form of gum disease that affects millions worldwide. It can lead to tooth loss and the destruction of supporting bone. This disease has also been linked to other health problems, including diabetes, respiratory infections, and heart disease, impacting quality of life and increasing health care costs.

Current treatments target bacterial infection and inflammation through nonsurgical therapies, such as scaling and root planing, commonly known as “deep cleaning.” However, they do not repair the gum’s extracellular matrix (ECM), the gingival tissue’s structural support that is damaged by chronic inflammation. Without this foundation, gingival tissue cannot function properly, allowing inflammation to persist and slowing healing.

Now, new research led by Kyle H. Vining and Hardik Makkar of the School of Dental Medicine demonstrates how the physical properties of the gingival tissue impact periodontal health and disease. Their findings are published in Advanced Materials.

How T cells amplify signals: New study reveals key molecular switch

Signaling is fundamental to how cells sense and respond to their environment—but in immune cells, those signals must be precisely amplified to mount an effective defense against invasive threats. New research by immunologists in Germany is shedding light on how that amplification occurs in T cells, revealing a key molecular mechanism that helps trigger immune responses—and may also contribute to inflammatory conditions.

Writing in Science Signaling, researchers at the University Medical Center Hamburg-Eppendorf identified a crucial step in the production of a “second messenger,” an internal signal that relays and amplifies messages received at the cell surface. Because external signaling molecules cannot enter the cell, second messengers translate those cues into powerful intracellular responses.

In T cells, that process depends on NAADP (nicotinic acid adenine dinucleotide phosphate), a molecule that drives calcium (Ca²⁺) signaling—an essential step in T cell activation. Without it, T cells cannot become the effector cells needed to fight serious threats, such as infections or cancer.

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