Innate immunity to mycobacterial infection in mice: critical role for toll-like receptors

Tuberculosis (Edinb). Sep-Nov 2005;85(5-6):395-405. doi: 10.1016/j.tube.2005.08.021. Epub 2005 Oct 27.

Abstract

Toll-like receptors (TLRs) play a critical role in the recognition of several pathogens, including Mycobacterium tuberculosis. Mycobacterial antigens recognize distinct TLRs resulting in rapid activation of cells of the innate immune system. Ablation of most of the TLR signalling as in mice deficient for the common adaptor protein MyD88 reveals that TLR is crucial for the activation of an innate immune response. MyD88-deficient mice are unable to clear virulent mycobacteria and succumb to acute necrotic pneumonia. Despite the profound defect of the innate immune response, MyD88 deficiency allows the emergence of an adaptive immunity. These data demonstrate that activation of multiple TLRs contributes to an efficient innate response to mycobacteria, while MyD88-dependent signalling is dispensable to generate adaptive immunity.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / immunology
  • Animals
  • Antigens, Bacterial / immunology*
  • Immunity, Active
  • Immunity, Innate*
  • Ligands
  • Mice
  • Mice, Knockout
  • Mycobacterium Infections / immunology*
  • Myeloid Differentiation Factor 88
  • Receptors, Cell Surface / immunology
  • Signal Transduction
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / immunology
  • Toll-Like Receptors / genetics
  • Toll-Like Receptors / immunology*

Substances

  • Adaptor Proteins, Signal Transducing
  • Antigens, Bacterial
  • Ligands
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Receptors, Cell Surface
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Mycobacterium tuberculosis antigens