Toll‐like receptor (TLR) signaling activates dendritic cells (DC) to secrete proinflammatory cytokines and up‐regulate co‐stimulatory molecule expression, thereby linking innate and adaptive immunity. A TLR‐associated adapter protein, MyD88, is essential for cytokine production induced by TLR. However, in response to a TLR4 ligand, lipopolysaccharide (LPS), MyD88‐deficient (MyD88^–/–) DC can up‐regulate co‐stimulatory molecule expression and enhance their T cell stimulatory activity, indicating that the MyD88‐independent pathway through TLR4 can induce some features of DC maturation. In this study, we have further characterized function of LPS‐stimulated, MyD88^–/– DC. In response to LPS, wild‐type DC could enhance their ability to induce IFN‐γ production in allogeneic mixed lymphocyte reaction (alloMLR). In contrast, in response to LPS, MyD88^–/– DC augmented their ability to induce IL‐4 instead of IFN‐γ in alloMLR. Impaired production of T_h1‐inducing cytokines in MyD88^–/– DC cannot fully account for their increased T_h2 cell‐supporting ability, because absence of T_h1‐inducing cytokines in DC caused impairment of IFN‐γ, but did not lead to augmentation of IL‐4 production in alloMLR. In vivo experiments with adjuvants also revealed T_h2‐skewed immune responses in MyD88^–/– mice. These results demonstrate that the MyD88‐independent pathway through TLR4 can confer on DC the ability to support T_h2 immune responses.