While mutations in human FOXP3 predispose individuals to autoimmune conditions, it is unclear how the mutant protein fails to function as a transcriptional regulator. There is also limited detail of how FOXP3 itself interacts with the transcriptional machinery and which components of the FOXP3 ensembles exert phenotypic changes to render cells able to mediate suppression. Increasing evidence indicates that the level and duration of FOXP3 expression plays a crucial role in the development and function of natural regulatory T cells (Tregs). Our studies focus on the post-translational modification of the FOXP3 protein, and how the FOXP3 complex ensemble, containing histone modification and chromatin-remodeling enzymes, defines its functional role in regulatory T cells. Understanding the molecular mechanisms underlying FOXP3 activity will provide therapeutic implications for transplantation, allergy, autoimmune disease and cancer.
Biochemistry and therapeutic implications of mechanisms involved in FOXP3 activity in immune suppression. Publishing Authors By Initials
Biochemistry and therapeutic implications of mechanisms involved in FOXP3 activity in immune suppression. Journal Published:
PUBLICATION TYPE: Review
Journal: Current opinion in immunology
VOLUME: 19
Page Numbers: 583-8
Journal Abbreviation: Curr. Opin. Immunol.
ISSN: 0952-7915
DAY: 20
MONTH: 08
YEAR: 2007
Biochemistry and therapeutic implications of mechanisms involved in FOXP3 activity in immune suppression. Information
Number of References: 53
LANGUAGE: eng
NlmUniqueID: 8900118
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Grant and Affiliation Information for Biochemistry and therapeutic implications of mechanisms involved in FOXP3 activity in immune suppression.
AFFILIATION: Department of Pathology and Laboratory Medicine, University of Pennsylvania, 252 John Morgan Building, 36th and Hamilton Walk, Philadelphia, PA 19104-6082, USA.
Country: England
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MEDLINETA: Curr Opin Immunol
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