Deletion of LTβR augments male susceptibility to Plasmodium chabaudi

Parasite Immunology

Volumn 27, Issue 6, 2005, Pages 205-212

  Krucken J ^a   Braun, J V ^a   Dkhil, M A ^b   Grunwald, A ^a   Wunderlich, Frank ^a  

^a HEINRICH HEINE UNIVERSITY   (Germany)

^b HELWAN UNIVERSITY   (Egypt)

Author keywords

Malaria; Microarray; plasmodium

Indexed keywords

GAMMA INTERFERON INDUCIBLE PROTEIN 10; HYDROXYSTEROID SULFOTRANSFERASE; LYMPHOTOXIN BETA; PHOSPHATASE; PLASMINOGEN ACTIVATOR INHIBITOR 1; PROTEIN DUAL SPECIFICITY PHOSPHATASE 1; PROTEIN HYDROXYSTEROID SPECIFIC SULFOTRANSFERASE SULT2A1; PROTEIN HYDROXYSTEROID SPECIFIC SULFOTRANSFERASE SULT2A2; PROTEIN LYMPHOTOXIN BETA RECEPTOR; RECEPTOR; TESTOSTERONE; UNCLASSIFIED DRUG; 3CH134 PROTEIN; ALPHA CHEMOKINE; CELL CYCLE PROTEIN; CXCL10 PROTEIN, MOUSE; IMMEDIATE EARLY PROTEIN; LTBR PROTEIN, MOUSE; LYMPHOTOXIN BETA RECEPTOR; MESSENGER RNA; PHOSPHOPROTEIN PHOSPHATASE; PROTEIN TYROSINE PHOSPHATASE; TUMOR NECROSIS FACTOR RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CASTRATION; CONTROLLED STUDY; DISEASE COURSE; DISEASE PREDISPOSITION; DISEASE SEVERITY; DNA MICROARRAY; FEMALE; GENE DELETION; GENE DISRUPTION; GENE EXPRESSION; IMMUNE RESPONSE; IMMUNOGENETICS; MALARIA; MALE; MOUSE; NONHUMAN; NORTHERN BLOTTING; PARASITEMIA; PLASMODIUM CHABAUDI; PRIORITY JOURNAL; SEX DIFFERENCE; SIGNAL TRANSDUCTION; SPLEEN; ANIMAL; BIOSYNTHESIS; C57BL MOUSE; GENE EXPRESSION REGULATION; GENETIC PREDISPOSITION; GENETICS; IMMUNOLOGY; LIVER; METABOLISM; MOUSE MUTANT; ORCHIECTOMY; PARASITOLOGY; PHYSIOLOGY;

PLASMODIUM CHABAUDI;

ANIMALS; CELL CYCLE PROTEINS; CHEMOKINES, CXC; FEMALE; GENE EXPRESSION REGULATION; GENETIC PREDISPOSITION TO DISEASE; IMMEDIATE-EARLY PROTEINS; LIVER; LYMPHOTOXIN BETA RECEPTOR; MALARIA; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; ORCHIECTOMY; PHOSPHOPROTEIN PHOSPHATASE; PLASMINOGEN ACTIVATOR INHIBITOR 1; PLASMODIUM CHABAUDI; PROTEIN-TYROSINE-PHOSPHATASE; RECEPTORS, TUMOR NECROSIS FACTOR; RNA, MESSENGER; SEX FACTORS; SPLEEN;

EID: 23444432701     PISSN: 01419838     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1365-3024.2005.00763.x     Document Type: Article

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