The Koch phenomenon and delayed hypersensitivity: 1891–1991
1991; Churchill Livingstone; Volume: 72; Issue: 1 Linguagem: Inglês
10.1016/0041-3879(91)90018-n
ISSN1878-6006
AutoresGrahamH. Bothamley, John M. Grange,
Tópico(s)Pediatric health and respiratory diseases
ResumoPurpose: Mycobacterium tuberculosis contributed to the discovery of delayed-type hypersensitivity and cell-mediated immunity. However, the biochemical basis for the immunogenicity of the mycobacterial cell wall has until recently remained unknown. Recent findings: Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) responds to bacterial peptidolycan-derived muramyl dipeptide (MDP). Whereas most bacteria produce N-acetyl MDP, mycobacteria produce an unusual modified form of MDP, called N-glycolyl MDP. Disruption of N-glycolyl MDP synthesis in mycobacteria greatly diminishes the contribution of NOD2 to mycobacterial sensing. Additionally, N-glycolyl MDP is more potent and efficacious than N-acetyl MDP at inducing innate responses and T cell-mediated immunity. Summary: The sensitivity of NOD2 to the mycobacterial peptidoglycan may link the natural history of both innate and adaptive immunity to mycobacterial infection.
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