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

被引:169
作者
Georgel, Philippe [2 ,3 ]
Radosavljevic, Mirjana [1 ,2 ]
Macquin, Cecile [2 ]
Bahram, Seiamak [1 ,2 ]
机构
[1] Hop Univ Strasbourg, Lab Cent Immunol, Nouvel Hop Civil, F-67091 Strasbourg, France
[2] Univ Strasbourg, Lab Immunogenet Mol Humaine, Ctr Rech Immunol & Hematol, Fac Med, F-67085 Strasbourg, France
[3] Univ Strasbourg, Fac Pharm, F-67401 Illkirch Graffenstaden, France
关键词
Innate immunity; MHC class I related; Klebsiella pneumoniae; INVARIANT T-CELLS; ACQUIRED-IMMUNITY; CYTOPLASMIC TAIL; EXPRESSION; RECEPTOR; INNATE; GENES; HEMOCHROMATOSIS; INTERLEUKIN-17; ASSOCIATION;
D O I
10.1016/j.molimm.2010.12.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 beta(2)microglobulin (beta(2)m)-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 beta(2)m 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. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:769 / 775
页数:7
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