Lack of interleukin-4 receptor α chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation inBalb/c mice

2008 ◽  
Vol 214 (5) ◽  
pp. 603-609 ◽  
Author(s):  
CWS Ko ◽  
RJ Cuthbert ◽  
NM Orsi ◽  
DA Brooke ◽  
SL Perry ◽  
...  
Keyword(s):  
Interleukin 4 ◽  
Aberrant Crypt Focus ◽  
Focus Formation ◽  
Α Chain ◽  
Interleukin 4 Receptor

Overexpression, Purification, and Use of a Soluble Human Interleukin-4 Receptor α-chain/Igγ1 Fusion Protein for Ligand Binding Studies

1997 ◽  
Vol 239 (2) ◽  
pp. 534-542 ◽  
Author(s):  
Irene Seipelt ◽  
Silke H. Hoffmann ◽  
Jürgen Schmidt ◽  
Joachim W. Engels ◽  
Thomas Beckers
Keyword(s):  
Fusion Protein ◽  
Ligand Binding ◽  
Interleukin 4 ◽  
Binding Studies ◽  
Α Chain ◽  
Interleukin 4 Receptor

Human eosinophils constitutively express the interleukin-4 receptor α-chain, involved in the induction of PI-3 kinase activity by IL-4 and IL-13

1997 ◽  
Vol 56 ◽  
pp. 36
Author(s):  
G.R. Dubois ◽  
R.C. Schweizer ◽  
C. Versluis ◽  
C.A.F.M. Bruijnzeel-Koomen ◽  
P.L.B. Bruijnzeel
Keyword(s):  
Kinase Activity ◽  
Interleukin 4 ◽  
Α Chain ◽  
Interleukin 4 Receptor

scholarly journals Homodimerization of Interleukin-4 Receptor α Chain Can Induce Intracellular Signaling

1996 ◽  
Vol 271 (39) ◽  
pp. 23634-23637 ◽  
Author(s):  
Winfried Kammer ◽  
Antje Lischke ◽  
Richard Moriggl ◽  
Bernd Groner ◽  
Andrew Ziemiecki ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Interleukin 4 ◽  
Α Chain ◽  
Interleukin 4 Receptor

Association of the Q576R polymorphism in the interleukin-4 receptor α chain with indolent mastocytosis limited to the skin

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 880-882 ◽  
Author(s):  
Trisha Daley ◽  
Dean D. Metcalfe ◽  
Cem Akin
Keyword(s):  
Mast Cell ◽  
Systemic Mastocytosis ◽  
Interleukin 4 ◽  
Gain Of Function ◽  
Cell Hyperplasia ◽  
Α Subunit ◽  
Disease Markers ◽  
Α Chain ◽  
Interleukin 4 Receptor ◽  
Mast Cell Hyperplasia

Abstract Gain-of-function mutations in c-kit, which appear to contribute to mast cell hyperplasia, have been detected in both limited and aggressive forms of mastocytosis, suggesting that other mutations or polymorphisms may contribute to the clinical phenotype. Because addition of interleukin-4 (IL-4) to mast cell cultures is reported to induce apoptosis, the hypothesis was considered that individuals carrying the gain-of-function polymorphism Q576R in the cytoplasmic domain of the α-subunit of the IL-4 receptor (IL-4R) might be relatively resistant to the gain-of-function mutation in c-kit. To assess this possibility, 36 patients with either cutaneous or systemic mastocytosis were studied for association with the Q576R polymorphism. The Q576R polymorphism was found more frequently in those with disease limited to skin and who exhibited lower levels of surrogate disease markers. These data suggest that the Q576R IL-4R α- chain polymorphism may mitigate disease expression and confer a better prognosis in patients with mastocytosis.

scholarly journals Signaling via Interleukin-4 Receptor α Chain Is Required for Successful Vaccination against Schistosomiasis in BALB/c Mice

2001 ◽  
Vol 69 (1) ◽  
pp. 228-236 ◽  
Author(s):  
Adrian P. Mountford ◽  
Karen G. Hogg ◽  
Patricia S. Coulson ◽  
Frank Brombacher
Keyword(s):  
Immune Responses ◽  
Protective Immunity ◽  
Interleukin 4 ◽  
Lymphoid Tissues ◽  
Partial Protection ◽  
Exposure Site ◽  
Ifn Γ ◽  
Α Chain ◽  
Interleukin 4 Receptor ◽  
Effector Response

ABSTRACT Although protective immunity in C57BL/6 mice induced by a single dose of the radiation-attenuated schistosome vaccine is believed to be mediated by Th1-type immune responses, we here report that in BALB/c mice protection can also depend upon signaling via the interleukin-4 (IL-4) receptor which conventionally governs the development of Th2-type immune responses. We show that in BALB/c mice deficient for the IL-4 receptor α chain (IL-4Rα−/−), which are unresponsive to IL-4 and IL-13, vaccine-induced protection is abrogated compared with that in wild-type (WT) mice. In vaccinated IL-4Rα−/− mice, IL-12p40 production by cells from the skin exposure site was elevated, although gamma interferon (IFN-γ) production in draining lymphoid tissues was similar in WT and IL-4Rα−/− mice. Nevertheless, the effector response in IL-4Rα−/− mice was Th1 biased with elevated IFN-γ in the lungs and higher immunoglobulin G2a (IgG2a) and IgG2b titers but negligible quantities of Th2-associated IgG1 and IgE. Interestingly, levels of IL-4 were equivalent in WT and IL-4Rα−/−mice, indicating that Th2 responses were not dependent upon signaling by IL-4 or IL-13. No differences in the phenotype and composition of the pulmonary effector mechanism that might explain the failure to induce protection in IL-4Rα−/− mice were detected. However, passive transfer of partial protection to naive IL-4Rα−/− mice, using serum from vaccinated WT mice, indicates that Th2-associated antibodies such as IgG1 have a role in parasite elimination in BALB/c strain mice and that signaling via IL-4R can be an important factor in the generation of protection.

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