{'fraction_non_alphanumeric': 0.03954802259887006, 'fraction_numerical': 0.011299435028248588, 'mean_word_length': 5.492146596858639, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
JAM‐A mediates leukocyte transmigration in a stimulus‐specific manner

Junctional adhesion molecule A (JAM‐A) is a transmembrane protein highly expressed at the tight junctions of endothelial and epithelial cells, as well as on the surface of platelets and leukocytes. Previous in vitro and in vivo work has implicated JAM‐A in leukocyte transmigration, though not all published data have been consistent. The present study aimed to further elucidate the role of JAM‐A in leukocyte transmigration in vivo. To address this objective, leukocyte transmigration through mouse cremasteric venules in response to LTB4, IL‐1β and ischaemia/reperfusion injury (I/R) was investigated by intravital microscopy using both a JAM‐A blocking mAb (BV‐11) and JAM‐A‐deficient (KO) mice. Leukocyte transmigration (but not adhesion) as stimulated by IL‐1β and I/R was almost totally blocked in animals treated with BV‐11 and a significant suppression was observed in JAM‐A KO animals (49 % inhibition, p<0.05). In contrast, neither JAM‐A blockade nor deletion had an effect on responses elicited by LTB4. The findings demonstrate that the ability of JAM‐A to mediate leukocyte transmigration is stimulus‐specific, a phenomenon previously found with PECAM‐1.