As a common group-occurring disease, endometritis is caused by endometrial cell injury and chronic inflammation of uteri infected by pathogenic microorganisms, and leads to reproductive failure in dairy cows. Changes in the immune response function of the uteri affect the occurrence and development of endometritis. It was recently discovered that exosomes act as a functional regulator secreted by a variety of cells. However, its regulatory mechanism in the local immune response of the uteri is still unclear. In this study, flow cytometry was adopted to identify that the number of T lymphocytes in the uteri with endometritis increased while the compositional proportion also changed, namely that of Tc cell increased very significantly and that of Th and Treg cells decreased very significantly. Moreover, the functional marker factor Foxp3 of Treg cells was extremely significantly decreased, and the functional marker factor of Th17 cells was significantly increased. The mRNA expression of immune tolerance regulators PD1, CTLA4 and Galectin-1 in the group of Treg cells which were co-incubated with LPS-stimulated endometrial epithelium-derived exosomes was very significantly lower than in the group of Treg cells which were co-incubated with normal EEC-derived exosomes. Furthermore, the protein expression of PD1, CTLA4, Galectin-1, Foxp3, and IL-17 was consistent with the results in the Treg cells co-incubated with different source exosomes in mice. Therefore, it was demonstrated that endometrial epithelium-derived exosomes act as a vital regulator of changes in the composition and function of T lymphocyte subsets in the uterus of dairy cows.