Inhibition of Major Histocompatibility Complex II Expression and Antigen Processing in Murine Alveolar Macrophages byMycobacterium bovisBCG and the 19-Kilodalton Mycobacterial Lipoprotein

• DOI: 10.1128/iai.72.4.2101-2110.2004
• Publication Date: 2004-03-23T22:43:10Z
• Authors: Scott A. Fulton; Scott M. Reba; Rish K. Pai; Meghan Pennini; Martha Torres; Clifford V. Harding; W. Henry Boom
• Keywords: CD86; CD80; Mycobacterium kansasii; CD11c

ABSTRACT Alveolar macrophages constitute a primary defense against Mycobacterium tuberculosis , but they are unable to control M. without acquired T-cell immunity. This study determined the antigen-presenting cell function of murine alveolar and ability model mycobacterium, bovis BCG, modulate it. The majority (80 85%) expressed both CD80 (B7.1) CD11c, 20 30% coexpressed major histocompatibility complex II (MHC-II). Gamma interferon (IFN-γ) enhanced MHC-II not B7.1 expression. Naive or IFN-γ-treated did express CD86 (B7.2), CD11b, Mac-3, CD40, F4/80. BCG 19-kDa mycobacterial lipoprotein inhibited IFN-γ-regulated expression on macrophages, inhibition was dependent Toll-like receptor 2. by associated with decreased presentation soluble antigen T cells. Thus, susceptibility may result from mycobacteria interfere macrophages.