PMID- 11929498
OWN - NLM
STAT- MEDLINE
DCOM- 20020802
LR  - 20190901
IS  - 0954-7894 (Print)
IS  - 0954-7894 (Linking)
VI  - 32
IP  - 2
DP  - 2002 Feb
TI  - Transforming growth factor-beta1 suppresses atopic dermatitis-like skin lesions 
      in NC/Nga mice.
PG  - 309-14
AB  - BACKGROUND: Atopic dermatitis is a chronic, relapsing inflammatory disorder 
      characterized by pruritic and eczematous skin lesions. Transforming growth factor 
      (TGF)-beta1 has been implicated in the suppression of inflammatory responses. 
      OBJECTIVE: The purpose of this study is to determine whether TGF-beta1 suppresses 
      skin lesions in a mouse model of atopic dermatitis. METHODS: We used the NC/Nga 
      strain of mice as an in vivo model of atopic dermatitis. The effects of exogenous 
      TGF-beta1 on atopic dermatitis-like skin lesions in NC/Nga mice were evaluated 
      clinically, histologically and immunologically. RESULTS: Subcutaneous injection 
      of recombinant TGF-beta1 macroscopically suppressed eczematous skin lesions in 
      NC/Nga mice associated with reduced serum immunoglobulin E (IgE) levels. 
      Histological analysis showed that TGF-beta1 significantly inhibited the 
      infiltration of inflammatory cells such as mast cells and eosinophils into the 
      skin of NC/Nga mice. Spontaneous interferon (IFN)-gamma production from 
      splenocytes of NC/Nga mice was down-regulated by the treatment with TGF-beta1 and 
      neutralizing antibody against IFN-gamma inhibited skin lesions in NC/Nga mice. 
      The inhibitory effect of TGF-beta1 on the skin lesions lasted at least 1 week 
      after cessation of the treatment. CONCLUSION: These findings indicate that 
      TGF-beta1 suppressed atopic dermatitis-like skin lesions in NC/Nga mice at least 
      in part through down-regulation of IFN-gamma. These results suggest that 
      TGF-beta1 may have a therapeutic potential for atopic dermatitis.
FAU - Sumiyoshi, K
AU  - Sumiyoshi K
AD  - Atopy (Allergy) Research Center Department of Dermatology, Juntendo University 
      School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
FAU - Nakao, A
AU  - Nakao A
FAU - Ushio, H
AU  - Ushio H
FAU - Mitsuishi, K
AU  - Mitsuishi K
FAU - Okumura, K
AU  - Okumura K
FAU - Tsuboi, R
AU  - Tsuboi R
FAU - Ra, C
AU  - Ra C
FAU - Ogawa, H
AU  - Ogawa H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Allergy
JT  - Clinical and experimental allergy : journal of the British Society for Allergy 
      and Clinical Immunology
JID - 8906443
RN  - 0 (Antibodies)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tgfb1 protein, mouse)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Dermatitis, Atopic/metabolism/*pathology
MH  - Disease Models, Animal
MH  - Immunoglobulin E/analysis
MH  - Interferon-gamma/antagonists & inhibitors/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Recombinant Proteins/pharmacology
MH  - Spleen/metabolism/pathology
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Transforming Growth Factor beta1
EDAT- 2002/04/04 10:00
MHDA- 2002/08/03 10:01
CRDT- 2002/04/04 10:00
PHST- 2002/04/04 10:00 [pubmed]
PHST- 2002/08/03 10:01 [medline]
PHST- 2002/04/04 10:00 [entrez]
AID - 1221 [pii]
AID - 10.1046/j.1365-2222.2002.01221.x [doi]
PST - ppublish
SO  - Clin Exp Allergy. 2002 Feb;32(2):309-14. doi: 10.1046/j.1365-2222.2002.01221.x.