The protein hormone adiponectin regulates glucose and fatty acid metabolism by binding to two PAQR-family receptors (AdipoR1 and AdipoR2). Both receptors feature a C-terminal segment which is released by proteolysis to form a freely circulating C-terminal fragment (CTF) found in the plasma of normal individuals but not in some undefined diabetes patients.

In the past decade, a tremendous progress has been made in developing T cell engaging bi-specific antibodies (BsAbs) targeting CD19 to treat B cell malignancies. The T cell engaging bi-specific molecule binds to CD3 on a T cell and a tumor-associated antigen (TAA) on a target cell and redirects the T cell to a specific target cell bypassing the MHC restriction mechanism, leading to the formation of immune synapse between the T cell and target cell and target cell lysis.

This study presents a comprehensive exploration into the shared molecular mechanisms linking psoriasis and major depressive disorder (MDD), two conditions that are increasingly recognized as having potential comorbidities. It offers new insights into the immune and genetic pathways that may contribute to both disorders, emphasizing the potential of CD19 as a biomarker and therapeutic target through the PPARγ/β-catenin/Wnt3a signaling pathway.

The complexity of the tumor microenvironment has been a challenge for understanding the mechanisms of therapy resistance. The development of improved animal models that closely mimic human disease is key for understanding and treating diseases. Recently, a new humanized mouse model has been developed that enables the study of human immune cells in tumor host-cell interactions

Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare and fatal premature aging disorder caused by progerin accumulation, leading to nuclear abnormalities, systemic inflammation, and early cardiovascular decline. Lonafarnib, a farnesyltransferase inhibitor (FTI), improves nuclear shape and extends lifespan, but its efficacy is limited and accompanied by pro-inflammatory effects. Here, we discuss preclinical findings from a combination therapy using the JAK1/2 inhibitor baricitinib (BAR) with FTI in a progeria mouse model.