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The non-conventional MHC class I MR1 molecule controls infection by Klebsiella pneumoniae in mice.

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Affiliations

  • 1. Laboratoire d'Immunogénétique Moléculaire Humaine, Centre de Recherche d'Immunologie et d'Hématologie, Faculté de Médecine, Université de Strasbourg, 4 rue Kirschleger, 67085 Strasbourg Cedex, France.
      Authors
    • Georgel P 1
    (1 author)

ORCIDs linked to this article

Molecular Immunology, 28 Dec 2010, 48(5):769-775
https://doi.org/10.1016/j.molimm.2010.12.002 PMID: 21190736 

Abstract 

As opposed to the well established role of MHC-linked, polymorphic, class I (MHC-I) genes in adaptive immunity, a universal role for non-conventional MHC-I is unknown, thus requiring a case-by-case study. The MHC unlinked, monomorphic, but β₂microglobulin (β₂m)-associated "MHC class I related" MR1 molecule interacts with a semi-invariant TCR. The pathophysiology of this interaction or more importantly of this peculiar MHC-I remains mostly unknown. Recently it was shown that β₂m deficient mice were more susceptible to infection by Klebsiella pneumoniae, a widely spread Gram-negative bacteria that causes diverse and often severe ailments in man. Here we demonstrate, using both an in vivo imaging system and survival tests, the increased susceptibility to K. pneumoniae (but not to several other Gram negative bacteria) of MR1 deficient mice. This is accompanied by a consequent change in body temperature and systemic cytokine profile. Hence MR1 controls K. pneumoniae infection in vivo.

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