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556 related items for PubMed ID: 7730635

  • 1. IL-12 is required for natural killer cell activation and subsequent T helper 1 cell development in experimental leishmaniasis.
    Scharton-Kersten T, Afonso LC, Wysocka M, Trinchieri G, Scott P.
    J Immunol; 1995 May 15; 154(10):5320-30. PubMed ID: 7730635
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  • 2. [TH1 response in the experimental infection with Trypanosoma cruzi].
    Cardoni RL, Antúnez MI, Abrami AA.
    Medicina (B Aires); 1999 May 15; 59 Suppl 2():84-90. PubMed ID: 10668248
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  • 8. TLR9 signaling is essential for the innate NK cell response in murine cutaneous leishmaniasis.
    Liese J, Schleicher U, Bogdan C.
    Eur J Immunol; 2007 Dec 15; 37(12):3424-34. PubMed ID: 18034422
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  • 9. IL-12 is essential for resistance against Yersinia enterocolitica by triggering IFN-gamma production in NK cells and CD4+ T cells.
    Bohn E, Autenrieth IB.
    J Immunol; 1996 Feb 15; 156(4):1458-68. PubMed ID: 8568248
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  • 10. Induction of a Th2 population from a polarized Leishmania-specific Th1 population by in vitro culture with IL-4.
    Mocci S, Coffman RL.
    J Immunol; 1995 Apr 15; 154(8):3779-87. PubMed ID: 7706719
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  • 11. T helper 1 response against Leishmania major in pregnant C57BL/6 mice increases implantation failure and fetal resorptions. Correlation with increased IFN-gamma and TNF and reduced IL-10 production by placental cells.
    Krishnan L, Guilbert LJ, Wegmann TG, Belosevic M, Mosmann TR.
    J Immunol; 1996 Jan 15; 156(2):653-62. PubMed ID: 8543817
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  • 12. Endogenous IL-12 is required for control of Th2 cytokine responses capable of exacerbating leishmaniasis in normally resistant mice.
    Heinzel FP, Rerko RM, Ahmed F, Pearlman E.
    J Immunol; 1995 Jul 15; 155(2):730-9. PubMed ID: 7608551
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  • 14. The mechanism of in vitro T helper cell type 1 to T helper cell type 2 switching in highly polarized Leishmania major-specific T cell populations.
    Mocci S, Coffman RL.
    J Immunol; 1997 Feb 15; 158(4):1559-64. PubMed ID: 9029090
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  • 15. Functional plasticity of the LACK-reactive Vbeta4-Valpha8 CD4(+) T cells normally producing the early IL-4 instructing Th2 cell development and susceptibility to Leishmania major in BALB / c mice.
    Maillard I, Launois P, Himmelrich H, Acha-Orbea H, Diggelmann H, Locksley RM, Louis JA.
    Eur J Immunol; 2001 Apr 15; 31(4):1288-96. PubMed ID: 11298356
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  • 16. IL-4 instructs TH1 responses and resistance to Leishmania major in susceptible BALB/c mice.
    Biedermann T, Zimmermann S, Himmelrich H, Gumy A, Egeter O, Sakrauski AK, Seegmüller I, Voigt H, Launois P, Levine AD, Wagner H, Heeg K, Louis JA, Röcken M.
    Nat Immunol; 2001 Nov 15; 2(11):1054-60. PubMed ID: 11600887
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  • 17. Early production of IL-4 and induction of Th2 responses in the lymph node originate from an MHC class I-independent CD4+NK1.1- T cell population.
    von der Weid T, Beebe AM, Roopenian DC, Coffman RL.
    J Immunol; 1996 Nov 15; 157(10):4421-7. PubMed ID: 8906817
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  • 18. Primed antigen-specific CD4+ T cells are required for NK cell activation in vivo upon Leishmania major infection.
    Bihl F, Pecheur J, Bréart B, Poupon G, Cazareth J, Julia V, Glaichenhaus N, Braud VM.
    J Immunol; 2010 Aug 15; 185(4):2174-81. PubMed ID: 20624944
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  • 19. Cellular and humoral immunity to Leishmania major in genetically susceptible mice after in vivo depletion of L3T4+ T cells.
    Sadick MD, Heinzel FP, Shigekane VM, Fisher WL, Locksley RM.
    J Immunol; 1987 Aug 15; 139(4):1303-9. PubMed ID: 3112230
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  • 20. The IL-4 rapidly produced in BALB/c mice after infection with Leishmania major down-regulates IL-12 receptor beta 2-chain expression on CD4+ T cells resulting in a state of unresponsiveness to IL-12.
    Himmelrich H, Parra-Lopez C, Tacchini-Cottier F, Louis JA, Launois P.
    J Immunol; 1998 Dec 01; 161(11):6156-63. PubMed ID: 9834101
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