Objective To investigate the effects of estrogen signaling on T-cell recruitment and polarization in acutely injured skeletal muscle.    Methods One hundred C57BL/6 male mice, one hundred and eighty C57BL/6 female mice were selected. Twenty-five female mice were ovariectomized (OVX) and 10 male mice were taken as the sham-operated (sham). Then, cardiotoxin(CTX) induced tibialis anterior(TA) injury for preparing mice myoinjury model. Subcutaneous injection of 17β-estradiol (E2) or estrogen receptor antagonist 4-hydroxytamoxifen (4-OHT) was performed. A total of 140 mice (70 males and 70 females) were divided into four group including: PBS-male, CTX-male, PBS-female, and CTX-female. Serum estradiol (E2) levels were measured by ELISA, and muscle injury models were validated via HE staining. Subsequently, 20 male and 20 female mice were selected for immunofluorescence (IF) and Real-time PCR to assess estrogen receptors (ER) expression in injured muscle tissue. Further, 10 male and 40 female mice were allocated into five experimental groups, including CTX, CTX+E2, CTX+4-OHT, CTX+OVX, CTX+sham. HE staining and IF were performed to evaluate inflammatory infiltration in the injured muscle. Additionally, 50 female mice were divided into CTX and CTX+OVX groups, and IF combined with flow cytometry were used to analyze T-cell phenotypes and muscle fiber regeneration in the injured muscle.    Results  In vivo, serum E2 and myofiber ERβ increased post-injury in mice of both sexes, significantly higher in females. Compared to the control group, E2 alleviated inflammation, OVX exacerbated inflammation, increased CD4^＋ T-cell infiltration, elevated T helper 1 cell(Th1) response, decreased regulatory T cells(Tregs), impaired regeneration. In vitro, IFN-γ/LPS significantly upregulated ERβ in myotubes.    Conclusion  Estrogen signaling critically regulates muscle inflammation. Estrogen deficiency (OVX) delays repair of skeletal muscle by promoting Th1 response and suppressing Tregs function.