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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

Variability between species is shown in the alignment of FoxP3 sequences of different mammalian species. FoxP3 sequences were obtained from the GenBank (http://www. ncbi.nlm.nih.gov/entrez). Sequences were aligned using the CLUSTALW profile alignment option. The resulting alignments were adjusted manually where necessary.
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fig02: Variability between species is shown in the alignment of FoxP3 sequences of different mammalian species. FoxP3 sequences were obtained from the GenBank (http://www. ncbi.nlm.nih.gov/entrez). Sequences were aligned using the CLUSTALW profile alignment option. The resulting alignments were adjusted manually where necessary.

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)

Variability between species is shown in the alignment of FoxP3 sequences of different mammalian species. FoxP3 sequences were obtained from the GenBank (http://www. ncbi.nlm.nih.gov/entrez). Sequences were aligned using the CLUSTALW profile alignment option. The resulting alignments were adjusted manually where necessary.
© Copyright Policy
Related In: Results  -  Collection

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

fig02: Variability between species is shown in the alignment of FoxP3 sequences of different mammalian species. FoxP3 sequences were obtained from the GenBank (http://www. ncbi.nlm.nih.gov/entrez). Sequences were aligned using the CLUSTALW profile alignment option. The resulting alignments were adjusted manually where necessary.
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