Correction of the iron overload defect in β-2-microglobulin knockout mice by lactoferrin abolishes their increased susceptibility to tuberculosis

Journal of Experimental Medicine

Volumn 196, Issue 11, 2002, Pages 1507-1513

  Schaible, Ulrich E ^a   Collins, Helen L ^a   Priem, Friedrich ^b   Kaufmann, Stefan H E ^a  

^a MAX PLANCK INSTITUTE FOR INFECTION BIOLOGY   (Germany)

^b HUMBOLDT UNIVERSITY   (Germany)

Author keywords

Endosomes; Innate immunity; Macrophages; MHC; Mycobacteria

Indexed keywords

BETA 2 MICROGLOBULIN; CD8 ANTIGEN; LACTOFERRIN; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 1; NITRIC OXIDE; REGULATOR PROTEIN; TRANSFERRIN RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; GENE MUTATION; HEMOCHROMATOSIS; HISTOCOMPATIBILITY; HISTOCOMPATIBILITY COMPLEX; HOST CELL; IMMUNE DEFICIENCY; IMMUNOCOMPETENT CELL; IMMUNOMODULATION; INFECTION RESISTANCE; INFECTION SENSITIVITY; IRON DEFICIENCY; IRON METABOLISM; IRON OVERLOAD; IRON TRANSPORT; KNOCKOUT MOUSE; MACROPHAGE; MOUSE; MOUSE STRAIN; MYCOBACTERIUM TUBERCULOSIS; NONHUMAN; PRIORITY JOURNAL; SEQUENCE HOMOLOGY; T LYMPHOCYTE; TUBERCULOSIS; WILD TYPE;

ANIMALS; BETA 2-MICROGLOBULIN; DISEASE SUSCEPTIBILITY; HISTOCOMPATIBILITY ANTIGENS CLASS I; INTERFERON TYPE II; IRON OVERLOAD; LACTOFERRIN; MACROPHAGES; MEMBRANE PROTEINS; MICE; MICE, KNOCKOUT; MYCOBACTERIUM TUBERCULOSIS; NITRIC OXIDE; RECEPTORS, TRANSFERRIN; TUBERCULOSIS;

EID: 0037011071     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.20020897     Document Type: Article

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