Invariant CD1d-restricted natural killer T cells play an important immunoregulatory role and can influence a broad spectrum of immunological responses including against bacterial infections. They are present at the fetal–maternal interface and although it has been reported that experimental systemic iNKT cell activation can induce mouse abortion, their role during pregnancy remain poorly understood. In the present work, using a physiological Chlamydia muridarum infection model, we have shown that, in vaginally infected pregnant mice, C. muridarum is cleared similarly in C57BL/6 wild type (WT) and CD1d−/− mice. We have also shown that infected- as well as uninfected-CD1d−/− mice have the same litter size as WT counterparts. Thus, CD1d-restricted cells are required neither for the resolution of chlamydial infection of the lower-genital tract, nor for the maintenance of reproductive capacity. However, unexpected differences in T cell populations were observed in uninfected pregnant females, as CD1d−/− placentas contained significantly higher percentages of CD4+ and CD8+ T cells than WT counterparts. However, infection triggered a significant decrease in the percentages of CD4+ T cells in CD1d−/− mice. In infected WT pregnant mice, the numbers of uterine CD4+ and CD8+ T cells, monocytes and granulocytes were greatly increased, changes not observed in infected CD1d−/− mice. An increase in the percentage of CD8+ T cells seems independent of CD1d-restricted cells as it occurred in both WT and CD1d−/− mice. Thus, in the steady state, the lack of CD1d-restricted NKT cells affects leukocyte populations only in the placenta. In Chlamydia-infected pregnant mice, the immune response against Chlamydia is dampened in the uterus. Our results suggest that CD1d-restricted NKT cells play a role in the recruitment or homeostasis of leukocyte populations at the maternal–fetal interface in the presence or absence of Chlamydia infection.