Mycoplasma fermentans-derived lipid inhibits class II major histocompatibility complex expression without mediation by interleukin-6, interleukin-10, tumor necrosis factor, transforming growth factor-β, type I interferon, prostaglandins or nitric oxide
✍ Scribed by Matthias Frisch; Gernot Gradehandt; Peter F. Mühlradt
- Book ID
- 102823999
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 844 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Mycoplasma fermentans-derived lipid inhibits class I1 major histocompatibility complex expression without mediation by interleukin-6, interleukin-10, tumor necrosis factor, transforming growth factor-p, type I interferon, prostaglandins or nitric oxide Mycoplasma cause several diseases in man and animals. Some strains can chronically infect humans, leading to fever or inflammatory syndromes such as arthritis, particularly in immunosuppressed patients. A set of pathogenicity factors shared by many mollicutes may be membrane components that activate macrophages to secrete cytokines and other inflammatory mediators. Mycoplasmaderived high molecular weight material (MDHM) is a macrophage-activating amphiphilic lipid which was purified from Mycoplasma fermentans. We studied the influence of MDHM on the expression of major histocompatibility complex (MHC) class I1 molecules by mouse resident peritoneal macrophages with an ELISA. Highly purified MDHM at 4 ng/ml and 0.8 pg/ml crude heat-killed M . fermentans (concentrations chosen to give maximal responses) suppresscd interferon (1FN)-y-dependent class I1 MHC induction when added simultaneously with IFN-y. MDHM was not toxic and did not result in loss of adherent cells. Kinetic data showed that MDHM first up-regulated, then down-regulated the expression of preformed class II MHC molecules, while expression of Mac-1 and F4/80 antigens rcmained constant. MDHM-dependent suppression of class I1 MHC molecule expression resulted in impaired antigen presentation to the helper T cell line D10.G4.1. We further attempted to identify hypothetical products of MDHM-stimulated macrophages as secondary mediators of class I1 MHC suppression such as were described for lipopolysaccharide (LPS)stimulated macrophages. Type I IFN, prostaglandins and nitric oxide, all reported to cause down-regulation of class I1 MHC, could be excluded in this context. Of the cytokines tumor necrosis factor, interleukin (1L)-6, IL-10 and transforming growth factor$, only IL-10 inhibited class I1 MHC expression, although less effectively than MDHM. The involvement of IL-10 was ruled out, as no evidence for its MDHM-dependent formation could be found. Our data suggest that MDHM interferes with class I1 MHC expression by up-regulating its turnover, and at the same time, inhibits the formation of new class I1 MHC molecules.