Comment on "Cigarette smoke-induced pulmonary inflammation is TLR4/MyD88 and IL-1R1/MyD88 signaling dependent"

J Immunol. 2008 May 1;180(9):5761; author reply 5761. doi: 10.4049/jimmunol.180.9.5761.
No abstract available

Publication types

  • Comment
  • Letter

MeSH terms

  • Animals
  • HSP70 Heat-Shock Proteins / genetics
  • HSP70 Heat-Shock Proteins / immunology
  • Humans
  • Immunity, Innate / genetics
  • Inflammation / etiology
  • Inflammation / genetics
  • Inflammation / immunology
  • Interleukin-1alpha / genetics
  • Interleukin-1alpha / immunology
  • Interleukin-1beta / genetics
  • Interleukin-1beta / immunology
  • Macrophages / immunology
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / immunology
  • Mice
  • Mice, Mutant Strains
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / immunology*
  • Neutrophils / immunology
  • Pneumonia / etiology
  • Pneumonia / genetics
  • Pneumonia / immunology*
  • Receptors, Interleukin-1 Type I / genetics
  • Receptors, Interleukin-1 Type I / immunology*
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • Smoking / adverse effects
  • Smoking / genetics
  • Smoking / immunology*
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / immunology*

Substances

  • HSP70 Heat-Shock Proteins
  • Interleukin-1alpha
  • Interleukin-1beta
  • Myeloid Differentiation Factor 88
  • Receptors, Interleukin-1 Type I
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Matrix Metalloproteinase 9