Targeting Opposing Immunological Roles of the Junctional Adhesion Molecule-A in Autoimmunity and Cancer

Frontiers in Immunology

Caio S. Bonilha¹  James M. Brewer¹  Paul Garside¹  Robert A. Benson² 

[1] College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom;Research and Development Department, Antibody Analytics Ltd., Newhouse, Lanarkshire, United Kingdom;

关键词: autoimmune diseases;    cell adhesion;    epithelial barrier;    F11 receptor;    inflammation;    junctional adhesion molecule-A;   

DOI  :  10.3389/fimmu.2020.602094

来源: DOAJ

【 摘 要 】

The junctional adhesion molecule-A (JAM-A) is a cell surface adhesion molecule expressed on platelets, epithelial cells, endothelial cells and leukocytes (e. g. monocytes and dendritic cells). JAM-A plays a relevant role in leukocyte trafficking and its therapeutic potential has been studied in several pathological conditions due to its capacity to induce leukocyte migration out of inflamed sites or infiltration into tumor sites. However, disruption of JAM-A pathways may worsen clinical pathology in some cases. As such, the effects of JAM-A manipulation on modulating immune responses in the context of different diseases must be better understood. In this mini-review, we discuss the potential of JAM-A as a therapeutic target, summarizing findings from studies manipulating JAM-A in the context of inflammatory diseases (e.g. autoimmune diseases) and cancer and highlighting described mechanisms.

【 授权许可】

Unknown