HMOX1 and asthma: Overexpression of HO-1 significantly inhibited the expression of activation marker CD200R and costimulatory factors, inhibited IL-4 release stimulated by DNP-OVA/anti-DNP-IgE, inhibited DQ-OVA up-taken both in the lung-derived BAs from asthma animal models and in cultured bone marrow-derived BAs, and subsequently, inhibited polarization of naïve T cells into Th2 cells in vitro and inhibited OVA-induced allergic airway inflammation and the Th2 immune response.