Trophoblast cell evades the maternal immune recognition by expressing non-classical (NC) MHC-I isoforms, in humans and mice. In the cow, MHC-I proteins are expressed from 120 d of pregnancy, however in clones MHC-I expression can begin as early as d 35. This abnormal expression of MHC-I in clones may play a role on high rates of embryo/fetal losses in this model. Our study aimed to determine expression of MHC-I and its NC isoforms in normal and cloned bovine pregnancy. Samples of normal and cloned bovine placenta in early (n = 5) and term (n = 6) pregnancy were used for immunolocalization of MHC-I by IHC, using antibodies for bovine MHC-I (IL-A88) and murine NC isoform (Qa-2). Also, the expression of classical MHC-I (JSP-1) and NC isoforms (NC1–4) was analyzed by qRT-PCR. Data were analyzed by least square ANOVA using the GLM procedure of SAS. The model included main effects (group and animal) and standard errors. In normal placenta, NC1 was equally expressed in early and late pregnancy, whereas in clones, NC1 tended to increase expression in late pregnancy (P = 0.07). NC2 was higher expressed during early pregnancy in clones than early normal pregnancy (P = 0.03) and both normal and clone late pregnancies (P = 0.04). For NC3 expression showed interaction between type and stage of pregnancy (P = 0.01). The expression of NC3 was higher in later in normal pregnancy (P < 0.01), while in clones the NC3 expression was higher in early stages (P = 0.04). Neither NC4 and JSP1 showed changes in expression among groups. Immunohistochemistry analysis showed that IL-A88 stained the maternal epithelium and non-invading trophoblast but not trophoblast giant cells. In early pregnancy, IL-A88 staining was weak in normal and almost absent in cloned placenta. At term, IL-A88 staining increased in normal placenta. For Qa-2, no staining was detected in early pregnancy in normal whereas the cloned placenta showed strong staining. Furthermore, in the term pregnancy the Qa-2 staining did not differ between normal and cloned placenta. Altogether, our data suggest that the MHC-I expression is dysregulated in clone pregnancy, which may contribute to their low pregnancy rates and success.