Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
 free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 free
 free
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Transforming growth factor-beta-induced regulatory T cells referee inflammatory and autoimmune diseases Wahl SM; Chen WArthritis Res Ther 2005[]; 7 (2): 62-8Naturally occurring CD4+CD25+ regulatory T cells mediate immune suppression to limit immunopathogenesis associated with chronic inflammation, persistent infections and autoimmune diseases. Their mode of suppression is contact-dependent, antigen-nonspecific and involves a nonredundant contribution from the cytokine transforming growth factor (TGF)-beta. Not only can TGF-beta mediate cell-cell suppression between the regulatory T cells and CD4+CD25- or CD8+ T cells, but new evidence also reveals its role in the conversion of CD4+CD25- T cells, together with TCR antigen stimulation, into the regulatory phenotype. Elemental to this conversion process is induction of expression of the forkhead transcription factor, Foxp3. This context-dependent coercion of naive CD4+ T cells into a powerful subset of regulatory cells provides a window into potential manipulation of these cells to orchestrate therapeutic intervention in diseases characterized by inadequate suppression, as well as a promising means of controlling pathologic situations in which excessive suppression dominates.|Animals[MESH]|Arthritis, Rheumatoid/immunology/therapy[MESH]|Asthma/therapy[MESH]|Autoimmune Diseases/*immunology[MESH]|CD4-Positive T-Lymphocytes/drug effects/*immunology[MESH]|CD8-Positive T-Lymphocytes/immunology[MESH]|Clonal Anergy[MESH]|Disease Models, Animal[MESH]|Forkhead Transcription Factors/biosynthesis/genetics[MESH]|Gene Expression Regulation[MESH]|Humans[MESH]|Immune Tolerance/immunology[MESH]|Immunotherapy, Adoptive[MESH]|Inflammation/*immunology[MESH]|Lupus Erythematosus, Systemic/immunology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Receptors, Interleukin-2/analysis[MESH]|Signal Transduction/physiology[MESH]|T-Lymphocytes, Regulatory/drug effects/*immunology/transplantation[MESH]|Transforming Growth Factor beta/*physiology[MESH] |
