3 results match your criteria: "Orleans University and CNRS[Affiliation]"
TNF in host resistance to tuberculosis infection.
Curr Dir Autoimmun
May 2010
Molecular Immunology and Embryology UMR6218, Orleans University and CNRS, Orleans, France.
TNF is essential to control Mycobacterium tuberculosis infection and cannot be replaced by other proinflammatory cytokines. Overproduction of TNF may cause immunopathology, while defective TNF production results in uncontrolled infection. The critical role of TNF in the control of tuberculosis has been illustrated recently by primary and reactivation of latent infection in some patients under pharmacological anti-TNF therapy for rheumatoid arthritis or Crohn's disease.
View Article and Find Full Text PDFMycobacterial phosphatidylinositol mannosides negatively regulate host Toll-like receptor 4, MyD88-dependent proinflammatory cytokines, and TRIF-dependent co-stimulatory molecule expression.
J Biol Chem
August 2009
Orleans University and CNRS, Molecular Immunology and Embryology, UMR6218, France.
Article Synopsis
- Mycobacterium tuberculosis uses special proteins and sugars to change how our immune system works.
- A specific sugar called PIM(6) or PIM(2) can reduce inflammation by stopping certain signals in our body from being released.
- This sugar shows promise for helping treat inflammation-related issues and could be used to develop new medicine to help with immune responses.
Acylation determines the toll-like receptor (TLR)-dependent positive versus TLR2-, mannose receptor-, and SIGNR1-independent negative regulation of pro-inflammatory cytokines by mycobacterial lipomannan.
J Biol Chem
September 2007
Orleans University and CNRS, Molecular Immunology and Embryology, UMR6218, 45071 Orléans, France.
Mycobacterium tuberculosis lipomannans (LMs) modulate the host innate immune response. The total fraction of Mycobacterium bovis BCG LM was shown both to induce macrophage activation and pro-inflammatory cytokines through Toll-like receptor 2 (TLR2) and to inhibit pro-inflammatory cytokine production by lipopolysaccharide (LPS)-activated macrophages through a TLR2-independent pathway. The pro-inflammatory activity was attributed to tri- and tetra-acylated forms of BCG LM but not the mono- and di-acylated ones.
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