Interleukin-4-deficient BALB/c mice develop an enhanced Th1-like response but control cardiac inflammation following Borrelia burgdorferi infection

FEMS Microbiology Letters

Volumn 183, Issue 2, 2000, Pages 319-325

  Satoskar, Abhay R ^a   Elizondo, Jennifer ^a   Monteforte, Gina M ^a   Stamm, Luisa M ^a   Bluethmann, Horst ^b   Katavolos, Paula ^a   Telford III, Sam R ^a  

^a HARVARD SCHOOL OF PUBLIC HEALTH   (United States)

^b F HOFFMANN LA ROCHE LTD   (Switzerland)

Author keywords

Borrelia burgdorferi; Carditis; Interleukin 4; Lyme disease

Indexed keywords

CYTOKINE; GAMMA INTERFERON; IMMUNOGLOBULIN G1; IMMUNOGLOBULIN G2A; INTERLEUKIN 10; INTERLEUKIN 4; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANTIBODY RESPONSE; ARTICLE; BORRELIA BURGDORFERI; CARDITIS; DISEASE SEVERITY; HISTOPATHOLOGY; LYME DISEASE; LYMPHOCYTE; LYMPHOCYTE PROLIFERATION; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

ANIMALS; ANTIBODIES, BACTERIAL; IMMUNOGLOBULIN G; INTERFERON TYPE II; INTERLEUKIN-10; INTERLEUKIN-4; LYME DISEASE; MICE; MICE, INBRED BALB C; MYOCARDITIS; TH1 CELLS;

EID: 0033976825     PISSN: 03781097     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0378-1097(00)00004-5     Document Type: Article

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