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Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis.

Rogier R, Koenders MI, Abdollahi-Roodsaz S - J Immunol Res (2015)

Bottom Line: However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors.However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood.A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

View Article: PubMed Central - PubMed

Affiliation: Experimental Rheumatology, Radboud University Medical Center, 6500 HB Nijmegen, Netherlands.

ABSTRACT
In autoimmune diseases, a disturbance of the balance between T helper 17 (Th17) and regulatory T cells (Tregs) is often observed. This disturbed balance is also the case in rheumatoid arthritis (RA). Genetic predisposition to RA confers the presence of several polymorphisms mainly regulating activation of T lymphocytes. However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors. Multiple studies have shown that commensal gut microbiota is of great influence on immune homeostasis and can trigger the development of autoimmune diseases by favoring induction of Th17 cells over Tregs. However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood. Here we review the current evidence supporting the involvement of commensal intestinal microbiota in rheumatoid arthritis, along with a potential role of Toll-like receptors (TLRs) in modulating the relevant Th cell responses to trigger autoimmunity. A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

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Exposure to deranged intestinal microbiota or a disregulated immune response to microbiota drives rheumatoid arthritis by promoting Th17 and deranging Treg cells.
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fig1: Exposure to deranged intestinal microbiota or a disregulated immune response to microbiota drives rheumatoid arthritis by promoting Th17 and deranging Treg cells.

Mentions: Most of the polymorphisms associated with RA are involved in regulating T cell activation [16]. The genetically altered T cells are potentially autoreactive, that is, they may react to self-antigens in the joint and cause autoimmunity; nevertheless, the “naïve” T cells (called Th0) first need to become activated and acquire a pathogenic phenotype in order to be harmful. Exposure to (deranged) intestinal microbiota may be a critical factor. The aim of this review is to discuss the role of intestinal bacteria in the development of RA in the context of T cell modulation and the possible role that TLRs play in this process (Figure 1).


Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis.

Rogier R, Koenders MI, Abdollahi-Roodsaz S - J Immunol Res (2015)

Exposure to deranged intestinal microbiota or a disregulated immune response to microbiota drives rheumatoid arthritis by promoting Th17 and deranging Treg cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4352938&req=5

fig1: Exposure to deranged intestinal microbiota or a disregulated immune response to microbiota drives rheumatoid arthritis by promoting Th17 and deranging Treg cells.
Mentions: Most of the polymorphisms associated with RA are involved in regulating T cell activation [16]. The genetically altered T cells are potentially autoreactive, that is, they may react to self-antigens in the joint and cause autoimmunity; nevertheless, the “naïve” T cells (called Th0) first need to become activated and acquire a pathogenic phenotype in order to be harmful. Exposure to (deranged) intestinal microbiota may be a critical factor. The aim of this review is to discuss the role of intestinal bacteria in the development of RA in the context of T cell modulation and the possible role that TLRs play in this process (Figure 1).

Bottom Line: However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors.However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood.A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

View Article: PubMed Central - PubMed

Affiliation: Experimental Rheumatology, Radboud University Medical Center, 6500 HB Nijmegen, Netherlands.

ABSTRACT
In autoimmune diseases, a disturbance of the balance between T helper 17 (Th17) and regulatory T cells (Tregs) is often observed. This disturbed balance is also the case in rheumatoid arthritis (RA). Genetic predisposition to RA confers the presence of several polymorphisms mainly regulating activation of T lymphocytes. However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors. Multiple studies have shown that commensal gut microbiota is of great influence on immune homeostasis and can trigger the development of autoimmune diseases by favoring induction of Th17 cells over Tregs. However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood. Here we review the current evidence supporting the involvement of commensal intestinal microbiota in rheumatoid arthritis, along with a potential role of Toll-like receptors (TLRs) in modulating the relevant Th cell responses to trigger autoimmunity. A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

Show MeSH
Related in: MedlinePlus