IL-12Rbeta2-deficient mice of a genetically resistant background are susceptible to Leishmania major infection and develop a parasite-specific Th2 immune response.

[1]  T. Mcclanahan,et al.  A Receptor for the Heterodimeric Cytokine IL-23 Is Composed of IL-12Rβ1 and a Novel Cytokine Receptor Subunit, IL-23R1 , 2002, The Journal of Immunology.

[2]  J. Berzofsky,et al.  Signals delivered through TCR instruct IL-12 receptor (IL-12R) expression: IL-12 and tumor necrosis factor-alpha synergize for IL-12R expression at low antigen dose. , 2001, International immunology.

[3]  M. Leach,et al.  Ubiquitous Transgenic Expression of the IL-23 Subunit p19 Induces Multiorgan Inflammation, Runting, Infertility, and Premature Death , 2001, The Journal of Immunology.

[4]  P. Launois,et al.  Interleukin (IL)-13 is the predominant Th2 cytokine in localized cutaneous leishmaniasis lesions and renders specific CD4+ T cells unresponsive to IL-12. , 2001, The Journal of infectious diseases.

[5]  C. Bogdan,et al.  Rapidly Fatal Leishmaniasis in Resistant C57BL/6 Mice Lacking TNF1 , 2001, The Journal of Immunology.

[6]  Xiaojing Ma TNF-α and IL-12:a balancing act in macrophage functioning , 2001 .

[7]  M. Martinetti,et al.  Humoral response to recombinant hepatitis B virus vaccine at birth: role of HLA and beyond. , 2000, Clinical immunology.

[8]  J. O’Shea,et al.  IL-12 Receptor β2 (IL-12Rβ2)-Deficient Mice Are Defective in IL-12-Mediated Signaling Despite the Presence of High Affinity IL-12 Binding Sites , 2000, The Journal of Immunology.

[9]  J Wagner,et al.  Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. , 2000, Immunity.

[10]  P. Scott,et al.  IL-12 Is Required to Maintain a Th1 Response During Leishmania major Infection1 , 2000, The Journal of Immunology.

[11]  F. Brombacher The role of interleukin‐13 in infectious diseases and allergy , 2000, BioEssays : news and reviews in molecular, cellular and developmental biology.

[12]  R. Locksley,et al.  In BALB/c Mice, IL-4 Production During the Initial Phase of Infection with Leishmania major Is Necessary and Sufficient to Instruct Th2 Cell Development Resulting in Progressive Disease1 , 2000, The Journal of Immunology.

[13]  J. Blackwell,et al.  IL-13 Is a Susceptibility Factor for Leishmania major Infection , 2000, The Journal of Immunology.

[14]  A. Satoskar,et al.  STAT‐4 mediated IL‐12 signaling pathway is critical for the development of protective immunity in cutaneous leishmaniasis , 1999, European journal of immunology.

[15]  D. Sacks,et al.  Inhibition of host cell signal transduction by Leishmania: observations relevant to the selective impairment of IL-12 responses. , 1999, Current opinion in microbiology.

[16]  C. Parra-López,et al.  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. , 1998, Journal of immunology.

[17]  P. Scott,et al.  Leishmania major-infected C3H mice treated with anti-IL-12 mAb develop but do not maintain a Th2 response. , 1997, Journal of immunology.

[18]  F. Mattner,et al.  Interleukin-12 is indispensable for protective immunity against Leishmania major , 1997, Infection and immunity.

[19]  S. Reed,et al.  Molecular cloning of a novel protein antigen of Leishmania major that elicits a potent immune response in experimental murine leishmaniasis. , 1996, Journal of immunology.

[20]  W. Solbach,et al.  IL-4-deficient Balb/c mice resist infection with Leishmania major , 1996, The Journal of experimental medicine.

[21]  J. Louis,et al.  Genetically resistant mice lacking interleukin‐12 are susceptible to infection with Leishmania major and mount a polarized Th2 cell response , 1996, European journal of immunology.

[22]  I. Müller,et al.  Susceptibility to Leishmania major Infection in Interleukin-4-Deficient Mice , 1996, Science.

[23]  R. Rerko,et al.  Endogenous IL-12 is required for control of Th2 cytokine responses capable of exacerbating leishmaniasis in normally resistant mice. , 1995, Journal of immunology.

[24]  G. Trinchieri,et al.  Dendritic cells produce IL-12 and direct the development of Th1 cells from naive CD4+ T cells. , 1995, Journal of immunology.

[25]  W. McMaster,et al.  The gene encoding streptothricin acetyltransferase (sat) as a selectable marker for Leishmania expression vectors. , 1995, Gene.

[26]  R. Locksley,et al.  Leishmania promastigotes evade interleukin 12 (IL-12) induction by macrophages and stimulate a broad range of cytokines from CD4+ T cells during initiation of infection , 1994, The Journal of experimental medicine.

[27]  G. Trinchieri,et al.  The adjuvant effect of interleukin-12 in a vaccine against Leishmania major , 1994 .

[28]  A. Sher,et al.  Interleukin 12 acts directly on CD4+ T cells to enhance priming for interferon gamma production and diminishes interleukin 4 inhibition of such priming. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[29]  R. Schaub,et al.  Resolution of cutaneous leishmaniasis: interleukin 12 initiates a protective T helper type 1 immune response , 1993, The Journal of experimental medicine.

[30]  R. Rerko,et al.  Recombinant interleukin 12 cures mice infected with Leishmania major , 1993, The Journal of experimental medicine.

[31]  Werner Müller,et al.  Interleukin‐4 transgenic mice of resistant background are susceptible to Leishmania major infection , 1993, European journal of immunology.

[32]  R. Locksley,et al.  Production of interferon gamma, interleukin 2, interleukin 4, and interleukin 10 by CD4+ lymphocytes in vivo during healing and progressive murine leishmaniasis. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[33]  F. Liew,et al.  Tumor necrosis factor-alpha synergizes with IFN-gamma in mediating killing of Leishmania major through the induction of nitric oxide. , 1990, Journal of immunology.

[34]  R. Crawford,et al.  Leishmania major amastigotes initiate the L-arginine-dependent killing mechanism in IFN-gamma-stimulated macrophages by induction of tumor necrosis factor-alpha. , 1990, Journal of immunology.

[35]  M. Strath,et al.  Eosinophilia in transgenic mice expressing interleukin 5 , 1990, The Journal of experimental medicine.

[36]  C. Bogdan,et al.  Tumor necrosis factor‐α in combination with interferon‐γ, but not with interleukin 4 activates murine macrophages for elimination of Leishmania major amastigotes , 1990 .

[37]  R. Locksley,et al.  Cure of murine leishmaniasis with anti-interleukin 4 monoclonal antibody. Evidence for a T cell-dependent, interferon gamma-independent mechanism , 1990, The Journal of experimental medicine.

[38]  I. G. Young,et al.  Molecular cloning, nucleotide sequence, and expression of the gene encoding human eosinophil differentiation factor (interleukin 5). , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[39]  F. Liew Cell-mediated immunity in experimental cutaneous Leishmaniasis. , 1986, Parasitology today.

[40]  W. Solbach,et al.  The host response to Leishmania infection. , 2000, Advances in immunology.

[41]  L Adorini,et al.  The interleukin-12/interleukin-12-receptor system: role in normal and pathologic immune responses. , 1998, Annual review of immunology.

[42]  G. Trinchieri Interleukin-12: a cytokine at the interface of inflammation and immunity. , 1998, Advances in immunology.

[43]  R. Locksley,et al.  The regulation of immunity to Leishmania major. , 1995, Annual review of immunology.

[44]  R. Coffman,et al.  TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. , 1989, Annual review of immunology.