Many antigens of Mycobacterium tuberculosis (Mtb) have immune-modulating effect, resulting in alteration towards Mtb-favoring immune environment. Although recent studies have reported increased number of plasmacytoid dendritic cell (pDC) and its negative role in generating type I infeterones (IFNs) during Mtb infection, their function and phenotype in Mtb pathogenesis need to be elucidated. Here, we treated LprG of Mtb lipoproteins, known for an innate immune modulator, during pDC differentiation with FMS-like tyrosinekinase-1 ligand (Flt3L). Interestingly, the number of pDCs (LprG-pDC) relatively increased in presence of LprG compared to that treated with Flt3L alone (natural pDC, npDC). In addition, LprG-pDCs markedly less produced type I IFNs and TNF-a than npDCs in response to CPG-ODNs. In contrast, abundant IL-10 secretion was observed in LprG-pDCs only. Next, we investigated whether LprG-Flt3L co-treatment induced phenotypic alteration on surface markers of pDCs and their effect on T cells. LprG-pDCs more expressed tolergoenic markers such as chemokine receptor (CCR) 9, indoleamine 2, 3-dioxygenase (IDO), and programmed death ligand-1 (PD-L1) than npDCs. Furthermore, LprG-pDC displayed limited ability to induce the proliferation of CD4+ T cell when stimulating with CPG-ODNs in both antigen-specific- and non-specific- manners. Notably, LprG-pDC generated CD4+CD25+FoxP3+ regulatory T cells in vitro in absence of TGF-β. In conclusion, LprG, one of immune-modulating Mtb lipoproteins, is functionally capable of endowing tolerogenic property to pDCs during the differentiation.