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T regulatory cells: aid or hindrance in the clearance of disease?

Coleman CA, Muller-Trutwin MC, Apetrei C, Pandrea I - J. Cell. Mol. Med. (2007 Nov-Dec)

Bottom Line: CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self.Since their discovery in the early 1970s, the role of CD4+ CD25+ Tregs in both autoimmune and infectious disease has continued to expand.In addition, advances made in the purification and manipulation of CD4+ CD25+ Tregs using new cell markers, techniques and antibodies are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, Tulane University Health Sciences Center, New Orleans, LA, USA.

ABSTRACT
CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self. Since their discovery in the early 1970s, the role of CD4+ CD25+ Tregs in both autoimmune and infectious disease has continued to expand. This review examines the recent advances on the role CD4+ CD25+ Tregs may be playing in various diseases regarding progression or protection. In addition, advances made in the purification and manipulation of CD4+ CD25+ Tregs using new cell markers, techniques and antibodies are discussed. Ultimately, an overall understanding of the exact mechanism which CD4+ CD25+ Tregs implement during disease progression will enhance our ability to manipulate CD4+ CD25+ Tregs in a clinically beneficial manner.

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Related in: MedlinePlus

A schematic view of the full-length 431 amino acid long human FoxP3 wild-type protein. The structural domains illustrated include those that have been found to be important in the proper functioning of the FoxP3 protein. The exon 2 isoform of the protein has recently been shown to function the same as the wild-type form [53]. In IPEX patients, the majority of genetic mutations found occur in the zinc finger, leucine zipper and FKH domain regions of the protein and this may be attributed to the requirement of these regions in the transcriptional repression capabilities of the FoxP3 protein [44]. Commercially available antibodies that react with FoxP3 from human and non-human primate are diagrammed under the epitopes that the respective antibody reacts against. PCH101, FJK-16s, 236A/E7, 150D/E4 and ebio7979 are available from eBioscience. 150D, 206D and 259D clones are available from Biolegend. ab2481 and ab10563 are available from Abcam.
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fig03: A schematic view of the full-length 431 amino acid long human FoxP3 wild-type protein. The structural domains illustrated include those that have been found to be important in the proper functioning of the FoxP3 protein. The exon 2 isoform of the protein has recently been shown to function the same as the wild-type form [53]. In IPEX patients, the majority of genetic mutations found occur in the zinc finger, leucine zipper and FKH domain regions of the protein and this may be attributed to the requirement of these regions in the transcriptional repression capabilities of the FoxP3 protein [44]. Commercially available antibodies that react with FoxP3 from human and non-human primate are diagrammed under the epitopes that the respective antibody reacts against. PCH101, FJK-16s, 236A/E7, 150D/E4 and ebio7979 are available from eBioscience. 150D, 206D and 259D clones are available from Biolegend. ab2481 and ab10563 are available from Abcam.

Mentions: It is becoming more apparent that FoxP3 is not only a phenotypic marker of CD4+ CD25+ Tregs, but it is also essential to their development and function [43]. Highly conserved in mammalian species (Fig. 2), the FoxP3 protein belongs to the forkhead/wingedhelix FoxP sub-family of transcriptional regulators that have been shown to operate as both transcriptional activators and/or repressors [41]. FoxP3 is 431 amino acid long protein that encodes for structural domains, such as a leucine zipper, C2H2 zinc finger and a forkhead (FKH) domain (Fig. 3). FoxP3, unlike other FoxP members, encodes its FKH domain at the C-terminus of the protein. Also, the proline rich N-terminus of the FoxP3 protein is considered undefined [48] (Fig. 3).


T regulatory cells: aid or hindrance in the clearance of disease?

Coleman CA, Muller-Trutwin MC, Apetrei C, Pandrea I - J. Cell. Mol. Med. (2007 Nov-Dec)

A schematic view of the full-length 431 amino acid long human FoxP3 wild-type protein. The structural domains illustrated include those that have been found to be important in the proper functioning of the FoxP3 protein. The exon 2 isoform of the protein has recently been shown to function the same as the wild-type form [53]. In IPEX patients, the majority of genetic mutations found occur in the zinc finger, leucine zipper and FKH domain regions of the protein and this may be attributed to the requirement of these regions in the transcriptional repression capabilities of the FoxP3 protein [44]. Commercially available antibodies that react with FoxP3 from human and non-human primate are diagrammed under the epitopes that the respective antibody reacts against. PCH101, FJK-16s, 236A/E7, 150D/E4 and ebio7979 are available from eBioscience. 150D, 206D and 259D clones are available from Biolegend. ab2481 and ab10563 are available from Abcam.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401294&req=5

fig03: A schematic view of the full-length 431 amino acid long human FoxP3 wild-type protein. The structural domains illustrated include those that have been found to be important in the proper functioning of the FoxP3 protein. The exon 2 isoform of the protein has recently been shown to function the same as the wild-type form [53]. In IPEX patients, the majority of genetic mutations found occur in the zinc finger, leucine zipper and FKH domain regions of the protein and this may be attributed to the requirement of these regions in the transcriptional repression capabilities of the FoxP3 protein [44]. Commercially available antibodies that react with FoxP3 from human and non-human primate are diagrammed under the epitopes that the respective antibody reacts against. PCH101, FJK-16s, 236A/E7, 150D/E4 and ebio7979 are available from eBioscience. 150D, 206D and 259D clones are available from Biolegend. ab2481 and ab10563 are available from Abcam.
Mentions: It is becoming more apparent that FoxP3 is not only a phenotypic marker of CD4+ CD25+ Tregs, but it is also essential to their development and function [43]. Highly conserved in mammalian species (Fig. 2), the FoxP3 protein belongs to the forkhead/wingedhelix FoxP sub-family of transcriptional regulators that have been shown to operate as both transcriptional activators and/or repressors [41]. FoxP3 is 431 amino acid long protein that encodes for structural domains, such as a leucine zipper, C2H2 zinc finger and a forkhead (FKH) domain (Fig. 3). FoxP3, unlike other FoxP members, encodes its FKH domain at the C-terminus of the protein. Also, the proline rich N-terminus of the FoxP3 protein is considered undefined [48] (Fig. 3).

Bottom Line: CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self.Since their discovery in the early 1970s, the role of CD4+ CD25+ Tregs in both autoimmune and infectious disease has continued to expand.In addition, advances made in the purification and manipulation of CD4+ CD25+ Tregs using new cell markers, techniques and antibodies are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, Tulane University Health Sciences Center, New Orleans, LA, USA.

ABSTRACT
CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self. Since their discovery in the early 1970s, the role of CD4+ CD25+ Tregs in both autoimmune and infectious disease has continued to expand. This review examines the recent advances on the role CD4+ CD25+ Tregs may be playing in various diseases regarding progression or protection. In addition, advances made in the purification and manipulation of CD4+ CD25+ Tregs using new cell markers, techniques and antibodies are discussed. Ultimately, an overall understanding of the exact mechanism which CD4+ CD25+ Tregs implement during disease progression will enhance our ability to manipulate CD4+ CD25+ Tregs in a clinically beneficial manner.

Show MeSH
Related in: MedlinePlus