PMID- 9635196
OWN - NLM
STAT- MEDLINE
DCOM- 19980916
LR  - 20190728
IS  - 0960-9822 (Print)
IS  - 0960-9822 (Linking)
VI  - 8
IP  - 11
DP  - 1998 May 21
TI  - Differences between IL-4R alpha-deficient and IL-4-deficient mice reveal a role 
      for IL-13 in the regulation of Th2 responses.
PG  - 669-72
AB  - Allergens and infections with parasitic helminths preferentially induced Th2 
      immune responses associated with elevated levels of serum immunoglobulin E (IgE) 
      and expansion of eosinophils and mast cells. Interleukin-4 (IL-4) is a key 
      cytokine in the differentiation of naive CD4+ T cells into Th2 cells, which 
      produce a panel of cytokines including IL-4, IL-5, IL-6, IL-9, IL-10, and IL-13 
      [1] and have been shown to trigger recovery from gastrointestinal nematodes [2]. 
      Nonetheless, mice deficient for IL-4 have been shown to develop residual Th2 
      responses [3-5] and can expel the nematode Nippostrongylus brasiliensis [6], 
      suggesting that there is a functional equivalent of IL-4 in these processes. 
      IL-13 is a cytokine that shares some, but not all, biological activities with 
      IL-4 [7,8]. There is now compelling evidence that IL-4 and IL-13 share receptor 
      components, including IL-4R alpha and IL-13R alpha 1 [9]. In order to dissect the 
      roles of IL-4 and IL-13 in the regulation of Th2 cells and in the response to 
      nematode infections, we looked for differences between mice deficient for either 
      the IL-4 gene or the IL-4R alpha gene. Unlike IL-4, IL-4R alpha was required for 
      control of N. brasiliensis, and Th2 development during infection--as 
      characterized by cytokine production, GATA-3 and surface CD30 expression--was 
      more severely affected in IL-4R alpha-/- mice than in IL-4-/- mice. Injection of 
      recombinant IL-13 induced worm expulsion in otherwise incompetent RAG2-/- mice. 
      Our results suggest that IL-13 regulates Th2 responses to nematode infection and 
      requires IL-4R alpha.
FAU - Barner, M
AU  - Barner M
AD  - Basel Institute for Immunology, Switzerland.
FAU - Mohrs, M
AU  - Mohrs M
FAU - Brombacher, F
AU  - Brombacher F
FAU - Kopf, M
AU  - Kopf M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Curr Biol
JT  - Current biology : CB
JID - 9107782
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (GATA3 Transcription Factor)
RN  - 0 (Gata3 protein, mouse)
RN  - 0 (Interleukin-13)
RN  - 0 (Ki-1 Antigen)
RN  - 0 (Rag2 protein, mouse)
RN  - 0 (Receptors, Interleukin-4)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Trans-Activators)
RN  - 0 (V(D)J recombination activating protein 2)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Animals
MH  - DNA-Binding Proteins/genetics/immunology/metabolism
MH  - Female
MH  - GATA3 Transcription Factor
MH  - Interleukin-13/pharmacology/*physiology
MH  - Interleukin-4/*deficiency/genetics/physiology
MH  - Ki-1 Antigen/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Nippostrongylus
MH  - Receptors, Interleukin-4/*deficiency/genetics/physiology
MH  - Recombinant Proteins/pharmacology
MH  - Strongylida Infections/genetics/immunology/therapy
MH  - Th2 Cells/*immunology
MH  - Trans-Activators/metabolism
EDAT- 1998/06/23 00:00
MHDA- 1998/06/23 00:01
CRDT- 1998/06/23 00:00
PHST- 1998/06/23 00:00 [pubmed]
PHST- 1998/06/23 00:01 [medline]
PHST- 1998/06/23 00:00 [entrez]
AID - S0960-9822(98)70256-8 [pii]
AID - 10.1016/s0960-9822(98)70256-8 [doi]
PST - ppublish
SO  - Curr Biol. 1998 May 21;8(11):669-72. doi: 10.1016/s0960-9822(98)70256-8.