Acute pulmonary and systemic inflammation induced by smoke inhalation is crucial to the outcome and complications of burn patient, and immune dysfunction is implicated in the development of organ injury. To reveal the immune cytokines change and immune cell interactions is helpful to know the immune response following smoke inhalation injury. We were analyzing hematoxylin-eosin (HE) staining of the lung tissues of Smoke inhalation mouse model, and detect the immune cytokine expression after 2,6,24,48,72 hours by The Real-Time qPCR. Flow cytometry was used to identify the expression of DC cells, T cells in the spleen, bone marrow derived-dendritic cells (BMDCs) and respective subtypes at 48h post inhalation. CCK-8 detected at the level of BMDCs on T cell proliferation in a mixed lymphocyte response. Smoke inhalation induced inflammation as evidenced by the significantly altered inflammatory constituent, including inflammatory cytokines and factors such as TNF-α, IFN-γ, IL-2, IL-4, RAGE, TLR4 and HMGB1, as well as inflammatory cells such as dendritic cells, regulatory T cells and BMDCs. Further research on BMDCs revealed that after smoke exposure, there was an increased expression of co-stimulatory molecules, such as CD80 and MHC-II, which aided T cell proliferation. We found that cytokines and immune cells get activation after smoke inhalation in the mouse model, and the activated BMDCs prompt the proliferation of normal T cells.