It is well documented that air pollutants exacerbate respiratory diseases, such as asthma (Brunekreef and Holgate, 2002). Diesel exhaust particles (DEP), which are major contributors to the level of airborne particles less than 2.5 micrometers in aerodynamic diameter (PM2.5) in urban areas, consist of a carbon core upon which are absorbed various compounds, including polyaromatic hydrocarbons (PAH), nitroaromatic hydrocarbons, heterocyclics, quinones, aldehydes, aliphatic hydrocarbons and heavy metals (Vouk and Piver, 1983;Draper, 1986 ABSTRACT -Diesel exhaust particles (DEP), a well-known air pollutant, exacerbate type I hypersensitivity conditions, such as asthma and pollen allergy. In this study, we examined the effect of diesel exhaust (DE) exposure on delayed-type hypersensitivity (DTH), a type IV hypersensitivity, induced with methyl-bovine serum albumin (mBSA) in C57BL/6 mice. Mice were exposed to DE containing DEP at a dose of 1.78 mg/m 3 in an inhalation chamber for 14 days. On Day 7, DTH mice and DE-exposed DTH -tial sensitization. On Day 14, mice were injected s.c. into one footpad with 20 μl of 10 mg/ml mBSA disfootpad swelling (%) was observed in DTH mice compared with normal control mice, and this swell--ther enhanced by DE exposure. DE exposure increased production of IL-17, which enhances local tischange was observed in the percentage of CD4 + CD25 + + T regulatory (Treg) cells in splenic lymphocytes following DE exposure. IL-6 production was increased by DE, and this would facilitate the differentiation of naïve T cells to IL-17-producing Th17 cells, while concomitantly suppressing the competing differentiation pathway to IL-10-producing Treg cells. Our results indicate that DE inhalation may, in