TNFRSF1A (TNF Receptor Superfamily Member 1A)

Structural modeling showed weak interactions with Toll-like receptors, and epitope analysis predicted low immunogenicity. These results suggest ZAM-MSC may offer a safer antimicrobial alternative, though all protein-level findings are based on computational predictions and require experimental validation.

sTNFR1 is associated with cognitive decline and tau-related selective neurodegeneration, but provides limited incremental predictive value beyond established risk factors; external validation and replication are warranted.

Patients with mild-to-moderate psoriasis treated with balinatunfib reported no severe or serious TEAEs and showed promising clinical responses, suggesting that further evaluation of TNFR1 signal inhibition in inflammatory diseases is warranted.

Furthermore, Tnfrsf1a expression showed a negative correlation with the success rate of long-term memory formation. These findings suggest the existence of adaptive mechanisms associated with long-term memory formation that act to suppress proinflammatory signaling pathways in the brain.

Importantly, low HDL is independently associated with elevated TNFR1 levels, suggesting that lipid metabolism, beyond glucose control, plays a critical role in DKD progression. Monitoring HDL levels and targeting dyslipidemia may aid in the early prevention and intervention of DKD.

Further in vitro investigations confirmed that human podocytes, exposed to TNFα donor plasma, demonstrated TNFR1 signaling driven injury profiles, a response that was ameliorated by infliximab. Our data provide evidence that monitoring plasma inflammation levels during donor management offers a window of opportunity to intervene and improve optimisation and quality of deceased donor organs.

PLAE is associated with sex-specific dysregulation of the CX3CL1/CX3CR1 axis and convergent neuroimmune-vascular signatures indicative of subclinical endothelial dysfunction. These associative findings support the hypothesis that fractalkine-pathway modulation may mitigate long-term neurobehavioral and cardiovascular vulnerability after PLAE, warranting causal testing.

See also the graphical abstract(Fig. 1).

Mechanistic analyses using immunoblotting, surface plasmon resonance, and molecular dynamics simulations demonstrated that TI-16 selectively disrupts tumor necrosis factor-alpha/tumor necrosis factor receptor 1 (TNF-α/TNFR1) interaction without altering TNF-α trimerization. By simultaneously suppressing apoptotic and necroptotic signaling, TI-16 overcomes key limitations of current biologics and represents a promising lead for the development of a novel class of orally available TNF-α-targeted therapeutics.

Our results suggest that TNFSF transcripts represent the main activated inflammatory pathway in the midbrains of people with schizophrenia, which overlaps somewhat with bipolar disorder. These findings highlight the need for anti-inflammatory interventions targeting TNF/TNFSF receptors to test for therapeutic benefits in psychiatric patients displaying elevated inflammation.

Our analysis confirmed previously identified functional sites and revealed new residues likely to contribute to the structural stability and dynamics of the complex. These findings provide a more comprehensive understanding of the molecular determinants of TNF signaling and offer a foundation for future experimental investigations into the receptor-ligand interface and membrane-mediated regulation.

This study provides novel insights into the therapeutic potential of FGL1 in inflammatory liver disorders by modulating macrophage function and promoting liver repair. These results highlight its potential as a novel anti-inflammatory therapeutic agent for the treatment of inflammatory liver diseases.