Abstract
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.
Highlights
The junctional adhesion molecule-A (JAM-A), called junctional adhesion molecule-1 (JAM-1), is a member of the immunoglobulin superfamily and received its first denomination as F11 receptor (F11R), a molecule expressed on the surface of human platelets [1]
Bone marrow-derived dendritic cells (DC) (BMDC) treated with antiJAM-A mAb, or originating from JAM-A knockout (KO) mice, showed increased random motility in vitro compared to their respective controls [8]. These JAM-A-deficient BMDCs expressed similar levels of maturation markers (CD80 and CD86), surface molecules related to DC migration (CD11a, CD11b, CD11c, CD62L, junctional adhesion molecule-B (JAM-B), and JAM-C) and antigen uptake capacity in comparison to WT BMDCs, suggesting that JAM-A may not participate in early stages of DC differentiation and maturation
To address if this increased susceptibility was mediated by the higher number of B and T cells found in the lamina propria of JAM-A-/- mice, JAM-A-deficient mice crossed to recombination activating gene 1 (RAG1) knockout animals lacking B and T cell development were investigated [43]
Summary
Received: 02 September 2020 Accepted: 02 November 2020 Published: 25 November 2020. Citation: Bonilha CS, Benson RA, Brewer JM and Garside P (2020) Targeting Opposing Immunological Roles of the Junctional Adhesion Molecule-A in Autoimmunity and Cancer. 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. Disruption of JAM-A pathways may worsen clinical pathology in some cases. 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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