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Journal ArticleDOI

Susceptibility to Leishmania major Infection in Interleukin-4-Deficient Mice

Nancy Noben-Trauth, +2 more
- 16 Feb 1996 - 
- Vol. 271, Iss: 5251, pp 987-990
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TLDR
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.
Abstract
Interleukin-4 (IL-4), a pleiotropic cytokine, is a major regulator of the immune system and is considered crucial for the development of T helper cell type 2 (TH2) responses. The susceptibility of BALB/c mice to infection with Leishmania major has been associated with a polarized TH2 response and an inability to down-modulate IL-4 production. The role of IL-4 in vivo was examined directly by disrupting the IL-4 gene in BALB/c embryonic stem cells. 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.

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Induction of th1 and th2 cd4+ t cell responses : the alternative approaches

TL;DR: The effects on Th priming of (a) using altered peptide ligands as antigens, (b) varying the dose of antigen, and (c) altering costimulatory signals are discussed.
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Induction of tumor immunity by removing CD25+CD4+ T cells: a common basis between tumor immunity and autoimmunity.

TL;DR: Removal of immunoregulatory CD25+4+ T cells can abrogate immunological unresponsiveness to syngeneic tumors in vivo and in vitro, leading to spontaneous development of tumor-specific effector cells as well as tumor-nonspecific ones.
Journal ArticleDOI

The immunology of susceptibility and resistance to Leishmania major in mice

TL;DR: Established models of T-helper-2-cell dominance in BALB/c mice infected with Leishmania major — involving the early production of interleukin-4 by a small subset of LeishMania-specific CD4+ T cells — have been refined by accumulating evidence that this response is not sufficient and, under some circumstances, not required to promote susceptibility.
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Periostin: A novel component of subepithelial fibrosis of bronchial asthma downstream of IL-4 and IL-13 signals

TL;DR: Periostin induced by IL-4/IL-13 shows promise in inhibiting subepithelial fibrosis in bronchial asthma and may contribute to this process by binding to other extracellular matrix proteins.
References
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Journal ArticleDOI

TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties.

TL;DR: Two types of cloned helper T cells are described, defined primarily by differences in the pattern of lymphokines ynthesized, and the different functions of the two types of cells and their lymphokine synthesis are discussed.
Journal ArticleDOI

Identification of a monoclonal antibody specific for a murine T3 polypeptide

TL;DR: Results identify T3-epsilon as a cell surface protein involved in the transduction of activation signals and can both activate and inhibit T-cell function.
Journal ArticleDOI

Reciprocal expression of interferon gamma or interleukin 4 during the resolution or progression of murine leishmaniasis. Evidence for expansion of distinct helper T cell subsets.

TL;DR: The inverse relationship of IFN-gamma and IL-4 gene expression during leishmaniasis may underlie the divergence of cellular and humoral immunity that occurs during chronic infection with Leishmania and possibly other intracellular parasites.
Journal ArticleDOI

Altered immune responses in mice lacking inducible nitric oxide synthase

TL;DR: The infected mutant mice developed a significantly stronger Thl type of immune response than the wild-type or heterozygous mice, and showed reduced nonspecific inflammatory response to carrageenin, and were resistant to lipopolysaccharide-induced mortality.
Journal ArticleDOI

The regulation of immunity to Leishmania major.

TL;DR: Use of the murine L. major model continues to elucidate new methods for vaccine development and suggests a promising system for identification of genes that determine susceptibility to infection.
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