Zay Yar Soe

TL;DR: It is proposed that α4β7-expressing T exosomes distribute themselves to the small intestine and modify the expression of microenvironmental tissues such that any subsequent lymphocyte homing is precluded, which may represent a novel mechanism by which excessive lymphocytes homing to the intestinal tissues is downsized.

TL;DR: The results suggest the potential involvements of the EV β2 integrin, as well as EV PD-L2 and solublePD-L1, in the septic pathogenesis that occurs with the systemic immune activation leading to multiple organ dysfunctions.

TL;DR: In this article, integrins represent the biologically and medically significant family of cell adhesion molecules that govern a wide range of normal physiology and are dynamically controlled via activation-dependent conformational changes regulated by the balance of intracellular activators and inactivators, such as Shank-associated RH domain interactor (SHARPIN) and integrin cytoplasmic domain-associated protein 1 (ICAP-1).

TL;DR: T-cells and T-cell exosomes engineered to lack talin-2 showed reduced binding to the integrin ligand ICam-1 and MAdCAM-1 compared with control T- cells and exosome, despite the fact that those T cells andExosomes express intact levels of the other isoform talin -1.

TL;DR: TMD123 (rhsTM), TMD1 or TMD3 is a promising treatment option for sepsis that attenuates integrin-dependent binding of leukocytes to VECs, and may inhibit the undesirable adhesion and migration of le Bukocyte to V ECs in sepsi.