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Utilizing regulatory T cells against rheumatoid arthritis.

Haque M, Fino K, Lei F, Xiong X, Song J - Front Oncol (2014)

Bottom Line: Other Foxp3(-) Treg cells include Tr1, Th3, CD8(+)CD28(-/-), and Qa1-restricted T cells; however, the contribution of these Treg cells to self-tolerance, immune homeostasis as well as preventing autoimmunity is not well defined.Here, we discuss the phenotypes and function of Foxp3(+) Treg cells and the potential use of such Treg cells against rheumatoid arthritis (RA).Of note, even though most expanded populations of Foxp3(+) Treg cells exhibit suppressive activity, tissue-associated or antigen-specific Treg cells appear superior in suppressing local autoimmune disorders such as RA.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, Pennsylvania State University College of Medicine , Hershey, PA , USA.

ABSTRACT
Regulatory T (Treg) cells are essential for normal immune surveillance systems, and their dysfunction leads to development of diseases, such as autoimmune disorders. CD4(+)CD25(+) Treg cells are well-known suppressive cells, which express the transcription factor Foxp3, are indispensable for the maintenance of immune self-tolerance and homeostasis by suppressing aberrant or excessive immune response. Other Foxp3(-) Treg cells include Tr1, Th3, CD8(+)CD28(-/-), and Qa1-restricted T cells; however, the contribution of these Treg cells to self-tolerance, immune homeostasis as well as preventing autoimmunity is not well defined. Here, we discuss the phenotypes and function of Foxp3(+) Treg cells and the potential use of such Treg cells against rheumatoid arthritis (RA). Of note, even though most expanded populations of Foxp3(+) Treg cells exhibit suppressive activity, tissue-associated or antigen-specific Treg cells appear superior in suppressing local autoimmune disorders such as RA. In addition, utilizing tissue-associated Foxp3(+) Treg cells from stem cells may stable Foxp3 expression and avoid induction of a potentially detrimental systemic immunosuppression.

No MeSH data available.


Related in: MedlinePlus

Suppressive mechanisms of Treg cells. Treg cells mediate their suppressive activity by direct cell–cell contact mediated by CTLA-4 on both Teffs and APCs, e.g., DCs. Suppressive cytokines (IL-10 and TGF-β) suppresses DC maturation and function. Treg cells also destroy Teffs through secreting perforin and granzyme-A.
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Figure 1: Suppressive mechanisms of Treg cells. Treg cells mediate their suppressive activity by direct cell–cell contact mediated by CTLA-4 on both Teffs and APCs, e.g., DCs. Suppressive cytokines (IL-10 and TGF-β) suppresses DC maturation and function. Treg cells also destroy Teffs through secreting perforin and granzyme-A.

Mentions: In addition, nTregs and iTreg cells can directly kill autologous target cells through a CD18 and perforin-dependent manner (41–43). Upon activation, nTreg cells predominantly express granzyme-A while iTreg cells express granzyme B. Both subtypes of Treg cells exhibit perforin-dependent cytotoxicity against a variety of autologous target cells, including CD4+ and CD8+ T cells, CD14+ monocytes, and DCs. The mechanism by which the Treg cell subsets recognize their targets is unclear; however, several lines of evidence suggest that it is an MHC/TCR independent process. The potential suppressive mechanisms of Treg cells are briefly described in Figure 1.


Utilizing regulatory T cells against rheumatoid arthritis.

Haque M, Fino K, Lei F, Xiong X, Song J - Front Oncol (2014)

Suppressive mechanisms of Treg cells. Treg cells mediate their suppressive activity by direct cell–cell contact mediated by CTLA-4 on both Teffs and APCs, e.g., DCs. Suppressive cytokines (IL-10 and TGF-β) suppresses DC maturation and function. Treg cells also destroy Teffs through secreting perforin and granzyme-A.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4125784&req=5

Figure 1: Suppressive mechanisms of Treg cells. Treg cells mediate their suppressive activity by direct cell–cell contact mediated by CTLA-4 on both Teffs and APCs, e.g., DCs. Suppressive cytokines (IL-10 and TGF-β) suppresses DC maturation and function. Treg cells also destroy Teffs through secreting perforin and granzyme-A.
Mentions: In addition, nTregs and iTreg cells can directly kill autologous target cells through a CD18 and perforin-dependent manner (41–43). Upon activation, nTreg cells predominantly express granzyme-A while iTreg cells express granzyme B. Both subtypes of Treg cells exhibit perforin-dependent cytotoxicity against a variety of autologous target cells, including CD4+ and CD8+ T cells, CD14+ monocytes, and DCs. The mechanism by which the Treg cell subsets recognize their targets is unclear; however, several lines of evidence suggest that it is an MHC/TCR independent process. The potential suppressive mechanisms of Treg cells are briefly described in Figure 1.

Bottom Line: Other Foxp3(-) Treg cells include Tr1, Th3, CD8(+)CD28(-/-), and Qa1-restricted T cells; however, the contribution of these Treg cells to self-tolerance, immune homeostasis as well as preventing autoimmunity is not well defined.Here, we discuss the phenotypes and function of Foxp3(+) Treg cells and the potential use of such Treg cells against rheumatoid arthritis (RA).Of note, even though most expanded populations of Foxp3(+) Treg cells exhibit suppressive activity, tissue-associated or antigen-specific Treg cells appear superior in suppressing local autoimmune disorders such as RA.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, Pennsylvania State University College of Medicine , Hershey, PA , USA.

ABSTRACT
Regulatory T (Treg) cells are essential for normal immune surveillance systems, and their dysfunction leads to development of diseases, such as autoimmune disorders. CD4(+)CD25(+) Treg cells are well-known suppressive cells, which express the transcription factor Foxp3, are indispensable for the maintenance of immune self-tolerance and homeostasis by suppressing aberrant or excessive immune response. Other Foxp3(-) Treg cells include Tr1, Th3, CD8(+)CD28(-/-), and Qa1-restricted T cells; however, the contribution of these Treg cells to self-tolerance, immune homeostasis as well as preventing autoimmunity is not well defined. Here, we discuss the phenotypes and function of Foxp3(+) Treg cells and the potential use of such Treg cells against rheumatoid arthritis (RA). Of note, even though most expanded populations of Foxp3(+) Treg cells exhibit suppressive activity, tissue-associated or antigen-specific Treg cells appear superior in suppressing local autoimmune disorders such as RA. In addition, utilizing tissue-associated Foxp3(+) Treg cells from stem cells may stable Foxp3 expression and avoid induction of a potentially detrimental systemic immunosuppression.

No MeSH data available.


Related in: MedlinePlus