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

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FRONTIERS IN IMMUNOLOGY
卷 11, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.602094

关键词

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

资金

  1. CAPES Foundation, an agency under the Ministry of Education of Brazil [88881.129556/2016-01]
  2. Arthritis Research UK (ARUK) programme [19788]
  3. Innovative Medicines Initiative EU [115142-2]
  4. Research into Inflammatory Arthritis Centre Versus Arthritis (RACE) [22072]

向作者/读者索取更多资源

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.

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