Innate immunity in host-microbial interactions: beyond B27 in the spondyloarthropathies

Curr Opin Rheumatol. 2002 Jul;14(4):373-82. doi: 10.1097/00002281-200207000-00007.

Abstract

The spondyloarthropathies are diseases influenced by genetic predisposition and, to a varying extent, infectious triggers. A causal role for bacterial infections is most clear for reactive arthritis. Recent insights into arthritogenic components of bacteria may set the stage for a better understanding of disease pathogenesis, the role of heat shock proteins in antigen processing and immune activation, and the adjuvant effect of CpG-DNA. Recent developments in the area of innate immunity broaden current concepts of genetically defined factors in host-pathogen interactions. In particular, the biology of toll-like receptors as important elements in the innate immune response to pathogens is being defined. These factors in innate immunity may have important implications for sequelae of infections, such as reactive arthritis.

Publication types

  • Review

MeSH terms

  • Animals
  • Antigens, Bacterial / immunology
  • Bacteria / pathogenicity*
  • Bacterial Infections / genetics
  • Bacterial Infections / immunology
  • DNA, Bacterial / analysis
  • Drosophila Proteins*
  • Genetic Predisposition to Disease*
  • HLA-B27 Antigen* / genetics
  • HLA-B27 Antigen* / immunology
  • Heat-Shock Proteins
  • Humans
  • Immunity, Innate*
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / immunology
  • Organisms, Genetically Modified
  • Rats
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / immunology
  • Spondylarthropathies* / genetics
  • Spondylarthropathies* / immunology
  • Spondylarthropathies* / microbiology
  • Toll-Like Receptors

Substances

  • Antigens, Bacterial
  • DNA, Bacterial
  • Drosophila Proteins
  • HLA-B27 Antigen
  • Heat-Shock Proteins
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Toll-Like Receptors