Affiliation: National Institutes of Health
- An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient miceN Noben-Trauth
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1892, USA
Proc Natl Acad Sci U S A 94:10838-43. 1997..These results indicate that an IL-4-independent, beta2-microglobulin-dependent pathway exists through which the CD62L-low CD4+ population has acquired IL-4-producing capacity in vivo, strongly suggesting that these cells are NK T cells...
- Schistosome-infected IL-4 receptor knockout (KO) mice, in contrast to IL-4 KO mice, fail to develop granulomatous pathology while maintaining the same lymphokine expression profileD Jankovic
Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
J Immunol 163:337-42. 1999..Taken together, these findings argue that tissue pathology in schistosomiasis requires, in addition to egg-specific CD4+ lymphocytes, a previously unrecognized IL-4Ralpha+ non-T cell effector population...
- Single cell analysis reveals that IL-4 receptor/Stat6 signaling is not required for the in vivo or in vitro development of CD4+ lymphocytes with a Th2 cytokine profileD Jankovic
Immunobiology Section, Laboratory of Parasitic Diseases, and Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 164:3047-55. 2000....
- IL-4- and IL-4 receptor-deficient BALB/c mice reveal differences in susceptibility to Leishmania major parasite substrainsN Noben-Trauth
Laboratories ofImmunology and Parasitology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 162:6132-40. 1999..major infection. The results with LV39 infection indicate that yet another unidentified factor is capable of causing susceptibility to L. major in the absence of IL-4 or IL-4 signaling...
- Conventional, naive CD4+ T cells provide an initial source of IL-4 during Th2 differentiationN Noben-Trauth
Laboratory of Immunology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 165:3620-5. 2000..These data show that conventional, naive CD4+ T cells may be considered as initial sources of IL-4 and, in the absence of IFN-gamma and IL-12, this IL-4 can induce Th2 polarization...
- Susceptibility to Leishmania major infection in the absence of IL-4N Noben-Trauth
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
Immunol Lett 75:41-4. 2000..major. Furthermore, IL-4Ralpha - / - mice reveal that the ability of L. major to escape immune clearance depends on the parasite substrain...
- A targeted mutation in the IL-4Ralpha gene protects mice against autoimmune diabetesD L Radu
Department of Microbiology, Mount Sinai Medical School, New York, NY 10029, USA
Proc Natl Acad Sci U S A 97:12700-4. 2000..Even as late as 270 days of age, mice homozygous for the targeted allele had no insulitis or only peri-insulitis. Thus, the inability to respond to IL-4 and/or IL-13 protects mice against IDDM in this model of autoimmunity...
- Lack of skin fibrosis in tight skin (TSK) mice with targeted mutation in the interleukin-4R alpha and transforming growth factor-beta genesT McGaha
Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
J Invest Dermatol 116:136-43. 2001....
- Interleukin-4 (IL-4) and IL-13 signaling pathways do not regulate Borrelia burgdorferi-induced arthritis in mice: IgG1 is not required for host control of tissue spirochetesM R Potter
Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA
Infect Immun 68:5603-9. 2000..Furthermore, the IgG1 isotype is not required to control B. burgdorferi cell numbers in tissues. These findings suggest the host defense against B. burgdorferi infection is not dependent on the Th1-Th2 paradigm of T-cell responses...
- Suppression of IgE responses in CD23-transgenic animals is due to expression of CD23 on nonlymphoid cellsM Payet-Jamroz
Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA
J Immunol 166:4863-9. 2001..FDCs that interface with B cells in the germinal center are a candidate for explaining this CD23-mediated IgE suppression...
- Susceptibility to Leishmania major infection in interleukin-4-deficient miceN Noben-Trauth
Jackson Laboratory, Bar Harbor, ME 04609, USA
Science 271:987-90. 1996..Despite the absence of IL-4, the genetically pure BALB/c mutant mice remained susceptible to L. major infection, showed no signs of lesion healing or parasite clearance, and did not switch to a TH1 phenotype...
- T helper cell type 1-associated and cytotoxic T lymphocyte-mediated tumor immunity is impaired in interleukin 4-deficient miceT Schuler
Max Delbruck Center for Molecular Medicine, 13122 Berlin, Germany
J Exp Med 189:803-10. 1999..Together, our results demonstrate a novel and previously unanticipated role of IL-4 for the generation of Th1-associated, CTL-mediated tumor immunity...
- IL-13, IL-4Ralpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensisJ F Urban
United States Department of Agriculture, Beltsville, Maryland 20705, USA
Immunity 8:255-64. 1998..Additional observations made in the course of these experiments demonstrate that Stat6 signaling is not required for IL-4 enhancement of IgG1 production and actually inhibits IL-4-induction of mucosal mastocytosis...
- The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 miceA Metwali
Department of Internal Medicine, University of Iowa, Iowa City 52242, USA
J Immunol 157:4546-53. 1996..Thus the production of IL-4 early in the inflammatory response is not the only factor preventing Th1 expression in inflammation...
- Efficient targeting of the IL-4 gene in a BALB/c embryonic stem cell lineN Noben-Trauth
Max Planck Insitut für Immunbiologie, Freiburg, Germany
Transgenic Res 5:487-91. 1996..Furthermore, the genetically pure BALB/c IL-4 deficient mice will aid in studying the role of IL-4 in several infectious disease models in which the BALB/c mouse is a susceptible strain...
- Cutting edge: IL-4 receptor expression by non-bone marrow-derived cells is required to expel gastrointestinal nematode parasitesJ F Urban
U S Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Immunology and Disease Resistance Laboratory, Beltsville, MD 20705, USA
J Immunol 167:6078-81. 2001..Thus, direct IL-4Ralpha signaling of nonimmune gastrointestinal cells may be generally required to induce worm expulsion, even when mast cell and T cell responses are also required...
- Effect of recombinant human IL-4 on tryptase, chymase, and Fc epsilon receptor type I expression in recombinant human stem cell factor-dependent fetal liver-derived human mast cellsH Z Xia
Department of Internal Medicine, Virginia Commonwealth University, Richmond 23298, USA
J Immunol 159:2911-21. 1997....
- Genetic mapping of the IL-12 alpha chain gene (Il12a) on mouse chromosome 3P A Schweitzer
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Mamm Genome 7:394-5. 1996
- The interleukin-12 beta subunit (p40) maps to mouse chromosome 11N Noben-Trauth
The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA
Mamm Genome 7:392. 1996