{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T04:20:26Z","timestamp":1793247626472,"version":"4.5.0"},"reference-count":57,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,8,15]],"date-time":"2025-08-15T00:00:00Z","timestamp":1755216000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background and objective<\/jats:title>\n                    <jats:p>Emerging evidence indicates that inflammation regulates cardiac remodeling and heart failure (HF). IL12\u03b2 is a subunit for proinflammatory cytokines IL12 and IL23. However, the effect of IL12\u03b2 inhibition on HF development and the underlying mechanism is not understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We determined the effect of pharmacological inhibition of IL12\u03b2 using IL12\u03b2 blocking antibody on transverse aortic constriction (TAC)-induced left ventricular (LV) inflammation and HF development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      IL12\u03b2 blocking antibody significantly attenuated TAC-induced LV immune cell infiltration, hypertrophy, fibrosis, dysfunction, and the consequent pulmonary inflammation and remodeling. More specifically, we found that IL12\u03b2 blocking antibody significantly attenuated TAC-induced LV and pulmonary infiltration of neutrophils, macrophages, CD11c\n                      <jats:sup>+<\/jats:sup>\n                      dendritic cells, CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells, and CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells. Moreover, IL12\u03b2 blocking antibody significantly suppressed the production of pro-inflammatory cytokine pro-IL1\u03b2 and IFN\u03b3 by macrophages and IFN\u03b3 by CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells and\/or CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings indicate that pharmacological inhibition of IL12\u03b2 effectively protected the heart from systolic overload-induced inflammation, remodeling, and dysfunction by reducing the proinflammatory signaling from both innate and adaptive immune responses.<\/jats:p>\n                  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