PMID- 16162681
OWN - NLM
STAT- MEDLINE
DCOM- 20060516
LR  - 20240413
IS  - 0017-5749 (Print)
IS  - 1468-3288 (Electronic)
IS  - 0017-5749 (Linking)
VI  - 55
IP  - 5
DP  - 2006 May
TI  - Transforming growth factor beta induced FoxP3+ regulatory T cells suppress Th1 
      mediated experimental colitis.
PG  - 671-80
AB  - BACKGROUND AND AIMS: The imbalance between effector and regulatory T cells plays 
      a central role in the pathogenesis of inflammatory bowel diseases. In addition to 
      the thymus, CD4+CD25+ regulatory T cells can be induced in the periphery from a 
      population of CD25- T cells by treatment with transforming growth factor beta 
      (TGF-beta). Here, we analysed the in vivo function of TGF-beta induced regulatory 
      T (Ti-Treg) cells in experimental colitis. METHODS: Ti-Treg cells were generated 
      in cell culture in the presence or absence of TGF-beta and tested for their 
      regulatory potential in experimental colitis using the CD4+CD62L+ T cell transfer 
      model. RESULTS: Ti-Treg cells significantly suppressed Th1 mediated colitis on 
      CD4+CD62L+ T cell transfer in vivo, as shown by high resolution endoscopy, 
      histology, immunohistochemistry, and cytokine analysis. Further analysis of in 
      vivo and in vitro expanded Ti-Treg cells showed that exogenous interleukin 2 
      (IL-2) was crucial for survival and expansion of these cells. CONCLUSION: Our 
      data suggest that regulatory Ti-Treg cells expand by TGF-beta and exogenous IL-2 
      derived from effector T cells at the site of inflammation. In addition to Tr1 and 
      thymic CD4+CD25+ T cells, peripheral Ti-Treg cells emerge as a class of 
      regulatory T cells with therapeutic potential in T cell mediated chronic 
      intestinal inflammation.
FAU - Fantini, M C
AU  - Fantini MC
AD  - Laboratory of Immunology, I Medical Clinic, Johannes Gutenberg University of 
      Mainz, Mainz, Germany.
FAU - Becker, C
AU  - Becker C
FAU - Tubbe, I
AU  - Tubbe I
FAU - Nikolaev, A
AU  - Nikolaev A
FAU - Lehr, H A
AU  - Lehr HA
FAU - Galle, P
AU  - Galle P
FAU - Neurath, M F
AU  - Neurath MF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050914
PL  - England
TA  - Gut
JT  - Gut
JID - 2985108R
RN  - 0 (Cytokines)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Foxp3 protein, mouse)
RN  - 0 (Transforming Growth Factor beta)
RN  - 126880-86-2 (L-Selectin)
SB  - IM
CIN - Gut. 2006 May;55(5):604-6. PMID: 16609133
MH  - Adoptive Transfer/*methods
MH  - Animals
MH  - CD4-Positive T-Lymphocytes/*immunology
MH  - Cell Proliferation
MH  - Colitis/immunology/*therapy
MH  - Cytokines/immunology
MH  - Forkhead Transcription Factors/*immunology
MH  - Immunohistochemistry
MH  - L-Selectin/immunology
MH  - Lymphocyte Activation
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, SCID
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - T-Lymphocytes, Regulatory/immunology
MH  - Th1 Cells/immunology
MH  - Transforming Growth Factor beta/*immunology
PMC - PMC1856126
COIS- Conflict of interest: None declared.
EDAT- 2005/09/16 09:00
MHDA- 2006/05/17 09:00
PMCR- 2009/05/01
CRDT- 2005/09/16 09:00
PHST- 2005/09/16 09:00 [pubmed]
PHST- 2006/05/17 09:00 [medline]
PHST- 2005/09/16 09:00 [entrez]
PHST- 2009/05/01 00:00 [pmc-release]
AID - gut.2005.072801 [pii]
AID - gt72801 [pii]
AID - 10.1136/gut.2005.072801 [doi]
PST - ppublish
SO  - Gut. 2006 May;55(5):671-80. doi: 10.1136/gut.2005.072801. Epub 2005 Sep 14.