Figure 9.

TSLP regulates immune cell response and facilitates cardiac repair after MI. TSLP expression is increased in infarcted hearts and originates primarily from cardiomyocytes in the infarct border zone. Compared to WT mice, Crlf2 ^-/- mice exhibited reduced survival rates, impaired cardiac function, and increased adverse ventricular remodeling after MI. Meanwhile, the absence of TSLP-TLSPR signaling results in decreased CD4⁺ T-cell activation and proliferation, reduced Treg cell number and a lower Treg/Tconv ratio, but increased myeloid cell infiltration and a higher Ly6C^high/Ly6C^low monocyte ratio.