Immune Responses in Interleukin 4-Deficient Mice

Brusselle, Guy; Gros, Graham Le; Köhler, Georges; Schultze, Nathalie; Koebel, Pascale; Kips, Johan; Pauwels, Romain; Bluethmann, Horst

doi:10.1016/b978-0-12-105760-2.50018-2

Cited by 3 publications

(1 citation statement)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown in vivo in Nippostrongylus brasiliensis-infected IL-4 mice that lymph-node-derived T cells show no increase in IL-4, IL-5 or IL-10 production up on stimulation, in contrast to T cells from infected wild-type littermates [9], This confirms that IL-4-knockout mice have a deficient Th2 cell response. We have previously reported that IL-4 is crucially important in the induction of allergic airway inflammation in this in vivo murine model, an effect that again appears to be mediated by a T-ccll-dependent…”

Section: Discussionsupporting

confidence: 69%

Importance of lnterleukin-4 and lnterleukin-12 in Allergen-Induced Airway Changes in Mice

Kips

Brusselle

Joos

et al. 1995

Int Arch Allergy Immunol

View full text Add to dashboard Cite

T helper 2 (Th2)-like cells are thought to play a crucial role in the pathogenesis of atopic asthma. In this study, we attempted to evaluate the in vivo effect of suppressing Th2 cell development on allergen-induced airway changes. Repeated exposure of actively sensitized C57B1/6 mice to aerosolized ovalbumin (OA) causes, in comparison to saline-exposed control animals, synthesis of specific IgE, increase of eosinophils in bronchoalveolar lavage fluid and airway hyperresponsiveness. These effects are not observed in OA-exposed, sensitized IL-4-knockout mice. Likewise, these effects are inhibited in OA-exposed C57B1/6 mice treated with IL-12 during initial antigen exposure. These results suggest that suppressing Th2 cell development in vivo might have profound inhibitory effects on allergen-induced airway changes.

show abstract

Section: Discussionsupporting

confidence: 69%

Importance of lnterleukin-4 and lnterleukin-12 in Allergen-Induced Airway Changes in Mice

Kips

Brusselle

Joos

et al. 1995

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

Interleukin-5 and its receptor: a drug target for eosinophilia associated with chronic allergic disease

Devos

Plaetinck

Cornelis

et al. 1995

Journal of Leukocyte Biology

View full text Add to dashboard Cite

A characteristic feature of chronic allergic diseases such as asthma is the increase in eosinophil numbers in the inflamed tissue. In light of its specificity for the development of eosinophils, interleukin-5 (IL-5) is considered the most important cytokine involved in the regulation of eosinophilia. Hence, an antagonist for IL-5 activity is a new target for drug discovery programs. We have examined the opportunity for both a random and a rational approach for the identification of such an antagonist. The elucidation of the structure of IL-5 and the initial structure/function analysis of the ligand/receptor complex constitute a first step towards the design of antagonistic compounds. The identification of a small compound by random screening able to inhibit the IL-5/IL-5 receptor interaction indicated an important domain in the receptor. We examine here protein-based IL-5 antagonists, such as IL-5-muteins, soluble IL-5 receptor constructs, and monoclonal antibodies, for their potential as IL-5/IL-5 receptor antagonists, and the use of a murine model of eosinophil airway inflammation for their evaluation.

show abstract

Integration of TCR and IL-4 signals through STAT6 and the regulation of IL-4 gene expression

Schmidt‐Weber

Rao

Lichtman

2000

Molecular Immunology

View full text Add to dashboard Cite

Immune Responses in Interleukin 4-Deficient Mice

Cited by 3 publications

References 59 publications

Importance of lnterleukin-4 and lnterleukin-12 in Allergen-Induced Airway Changes in Mice

Importance of lnterleukin-4 and lnterleukin-12 in Allergen-Induced Airway Changes in Mice

Interleukin-5 and its receptor: a drug target for eosinophilia associated with chronic allergic disease

Integration of TCR and IL-4 signals through STAT6 and the regulation of IL-4 gene expression

Contact Info

Product

Resources

About