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Contact activation of Factor XII can initiate the plasma kallikrein\u2010kinin cascade, producing inflammation and angioedema. The role of Factor XII in psoriasis is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>The effects of deficiency of Factor XII or its enzymatic substrate, prekallikrein, were examined in the imiquimod\u2010induced mouse model of psoriasis. Skin microcirculation was assessed using intravital confocal microscopy and laser Doppler flowmeter. A novel antibody blocking Factor XII activation was evaluated for psoriasis prevention.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Expression of Factor XII was markedly up\u2010regulated in human and mouse psoriatic skin. Genetic deletion of Factor XII or prekallikrein, attenuated imiquimod\u2010induced psoriatic lesions in mice. Psoriatic induction increased skin microvascular blood perfusion, causing vasodilation, hyperpermeability and angiogenesis. It also promoted neutrophil\u2010vascular interaction, inflammatory cytokine release and enhanced Factor XII \/ prekallikrein enzymatic activity with elevated bradykinin. Factor XII or prekallikrein deficiency ameliorated these microvascular abnormalities and abolished bradykinin increase. Antagonism of bradykinin B\n                      <jats:sub>2<\/jats:sub>\n                      receptors reproduced the microvascular protection of Factor XII \/ prekallikrein deficiency, attenuated psoriatic lesions, and prevented protection by Factor XII \/ prekallikrein deficiency against psoriasis. Furthermore, treatment of mice with Factor XII antibody alleviated experimentally induced psoriasis and suppressed microvascular inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>Activation of Factor XII promoted psoriasis via prekallikrein\u2010dependent formation of bradykinin, which critically mediated psoriatic microvascular inflammation. Inhibition of contact activation represents a novel therapeutic strategy for psoriasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.16428","type":"journal-article","created":{"date-parts":[[2024,6,14]],"date-time":"2024-06-14T02:59:33Z","timestamp":1718333973000},"page":"3760-3778","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Factor XII and prekallikrein promote microvascular inflammation and psoriasis in mice"],"prefix":"10.1111","volume":"181","author":[{"given":"Yurong","family":"Zhang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zengrong","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of 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