CD112 Regulates Angiogenesis and T Cell Entry into the Spleen

Area of Science:

• Immunology
• Cell Biology
• Vascular Biology

Background:

• Junctional adhesion proteins control angiogenesis, vascular permeability, and leukocyte trafficking.
• CD112 (nectin-2) interacts with endothelial cells and leukocytes, with prior in vitro studies suggesting roles in cell migration and proliferation.

Purpose of the Study:

• To elucidate the in vivo role of CD112 in endothelial cell biology and leukocyte trafficking.
• To investigate the function of CD112 in angiogenesis and T cell homing.

Main Methods:

• Expression analysis of CD112 in murine tissues.
• Phenotypic analysis of CD112-deficient mice, focusing on retinal and splenic vascularization.
• In vitro studies using CD112 blockade to assess endothelial cell migration, tube formation, and T cell transmigration.
• Assessment of T cell homing to the spleen in CD112-deficient mice.

Main Results:

• CD112 is expressed by lymphatic and blood endothelial cells in mice.
• CD112 deficiency led to enhanced blood vessel coverage in the retina and spleen.
• CD112 blockade modulated endothelial cell migration and enhanced tube formation in vitro.
• Antibody blockade of CD112 reduced T cell transmigration across endothelial monolayers.
• T cell homing to the spleen was significantly reduced in CD112-deficient mice.

Conclusions:

• CD112 acts as a regulator of angiogenic processes in vivo.
• CD112 plays a novel role in controlling T cell entry into the spleen.