PMID- 15546390
OWN - NLM
STAT- MEDLINE
DCOM- 20050405
LR  - 20051117
IS  - 0105-2896 (Print)
IS  - 0105-2896 (Linking)
VI  - 202
DP  - 2004 Dec
TI  - Induction of allergic inflammation by interleukin-18 in experimental animal 
      models.
PG  - 115-38
AB  - Interleukin-18 (IL-18) has been regarded as a proinflammatory cytokine because of 
      its potent interferon-gamma-inducing activity. However, mutant mice that release 
      excess amounts of IL-18 spontaneously develop pruritic chronic dermatitis-like 
      atopic dermatitis (AD), suggesting the importance of IL-18 for the development of 
      AD. Intriguingly, depletion of il-18 but not stat6, an essential transcriptional 
      factor for IL-4 signaling, rescues the mice from AD, indicating IL-18-dependent, 
      T-helper 2 (Th2) cell-independent AD. This type of AD is classified as 
      innate-type allergy in contrast to Th2 cell-dependent ordinary allergy. 
      Consistent with the previous studies, mice transferred with antigen-specific Th1 
      cells exhibit no airway hyperresponsiveness and respiratory eosinophilic 
      inflammation after challenge with antigen alone. However, they suffer from asthma 
      upon challenge with antigen plus IL-18, with comparable levels of both the 
      alterations as in those transferred with Th2 cells following challenge with 
      antigen. The former type of asthma is categorized as Th1-associated allergy. 
      Therefore, it is definitely necessary to evaluate whether individual allergic 
      disorders involve either of these IL-18-mediated pathways or a Th2-mediated one.
FAU - Tsutsui, Hiroko
AU  - Tsutsui H
AD  - Department of Immunology & Medical Zoology, Hyogo College of Medicine, 
      Nishinomiya, Japan.
FAU - Yoshimoto, Tomohiro
AU  - Yoshimoto T
FAU - Hayashi, Nobuki
AU  - Hayashi N
FAU - Mizutani, Hitoshi
AU  - Mizutani H
FAU - Nakanishi, Kenji
AU  - Nakanishi K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
RN  - 0 (Interleukin-18)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Toll-Like Receptors)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Hypersensitivity/*immunology/*metabolism
MH  - Inflammation/*immunology/*metabolism
MH  - Interleukin-18/chemistry/genetics/immunology/*metabolism
MH  - Membrane Glycoproteins/immunology/metabolism
MH  - Receptors, Cell Surface/immunology/metabolism
MH  - Signal Transduction/immunology/physiology
MH  - Toll-Like Receptors
RF  - 243
EDAT- 2004/11/18 09:00
MHDA- 2005/04/06 09:00
CRDT- 2004/11/18 09:00
PHST- 2004/11/18 09:00 [pubmed]
PHST- 2005/04/06 09:00 [medline]
PHST- 2004/11/18 09:00 [entrez]
AID - IMR205 [pii]
AID - 10.1111/j.0105-2896.2004.00205.x [doi]
PST - ppublish
SO  - Immunol Rev. 2004 Dec;202:115-38. doi: 10.1111/j.0105-2896.2004.00205.x.