American Journal of Biochemistry and Biotechnology

Suppression of Basal and Cytokine Induced Expression of MHC, ICAM 1 and B7 Markers on Mouse Lung Epithelial Cells Exposed to Diesel Exhaust Particles

Rajiv K. Saxena, Wanda Williams and M. Ian Gilmour

DOI : 10.3844/ajbbsp.2007.187.192

American Journal of Biochemistry and Biotechnology

Volume 3, Issue 4

Pages 187-192


Diesel exhaust particles (DEP) constitute a significant component of airborne particulates in urban environment. Exposure to DEP is known to enhance susceptibility to viral and bacterial infections. We hypothesized that DEP could partially exert its effect on disease susceptibility by interfering with antigen presentation required for the generation of protective adaptive immune responses. MHC class I and class II molecules, ICAM 1 (CD54) and B7.1 (CD80) are intimately involved with the presentation of viral and bacterial antigens to T cells. In the present study we examined the effect of in vitro exposure to DEP on basal and cytokine induced expression levels of these key molecules on mouse lung epithelial cells. LA4 and TC1 mouse epithelial cell lines were activated with a cytokine mixture comprising IFNγ, TNFα and IL1β, in the presence or absence of DEP. CM significantly boosted the expression of MHC I and ICAM 1 antigens on epithelial cells. Exposure to DEP significantly inhibited the basal and CM induced expression of MHC I and ICAM 1 expression, but did not interfere with the constitutive expression of B7.1 on epithelial cells. Significant expression of MHC II antigens, which is needed for presentation of exogenous antigenic peptides, was not detected on either LA4 or TC1 cells. These results suggest that DEP may interfere with the expression of the cellular markers involved in the presentation of viral antigens.


© 2007 Rajiv K. Saxena, Wanda Williams and M. Ian Gilmour. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.