A novel chitosan-peptide system for cartilage tissue engineering with adipose-derived stromal cells.

The natural healing process of cartilage injuries often fails to fully restore the tissue's biological and mechanical functions. Cartilage grafts are costly and require surgical intervention, often associated with complications such as intraoperative infection and rejection by the recipient due to ischemia. Novel tissue engineering technologies aim to ideally fill the cartilage defect to prevent disease progression or regenerate damaged tissue.

Targeting BTLA with the peptide inhibitor HVEM(14-39) - A new way to restore the activity of T cells in melanoma.

The complex of B- and T-lymphocyte attenuator (BTLA) and herpes virus entry mediator (HVEM) plays a critical role in immune regulation and has emerged as a promising therapeutic target for cancer treatment. In this study, we investigated the potential of the peptide inhibitor HVEM(14-39) to restore peripheral T cell activity in patients with advanced melanoma. In these patients, CD8+ T cells downregulated BTLA expression and increased HVEM expression upon activation.

Peptide-based inhibitors targeting the PD-1/PD-L1 axis: potential immunotherapeutics for cancer.

The PD-1/PD-L1 complex belongs to the group of inhibitory immune checkpoints and plays a critical role in immune regulation. The PD-1/PD-L1 axis is also responsible for immune evasion of cancer cells, and this complex is one of the main targets of immunotherapies used in oncology. Treatment using immune checkpoint inhibitors is mainly based on antibodies.

Development and evaluation of RADA-PDGF2 self-assembling peptide hydrogel for enhanced skin wound healing.

Wound healing complications affect numerous patients each year, creating significant economic and medical challenges. Currently, available methods are not fully effective in the treatment of chronic or complicated wounds; thus, new methods are constantly sought. Our previous studies showed that a peptide designated as PDGF2 derived from PDGF-BB could be a promising drug candidate for wound treatment and that RADA16-I can serve as a release system for bioactive peptides in wound healing.

Why does the herpes simplex 1 virus-encoded UL49.5 protein fail to inhibit the TAP-dependent antigen presentation?

Herpes simplex virus 1 (HSV-1) is a well-studied herpesvirus that causes various human diseases. Like other herpesviruses, HSV-1 produces the transmembrane glycoprotein N (gN/UL49.5 protein), which has been extensively studied, but its function in HSV-1 remains largely unknown.