IL-17 and the Th17 lineage in systemic lupus erythematosus

@article{GarrettSinha2008IL17AT,
  title={IL-17 and the Th17 lineage in systemic lupus erythematosus},
  author={Lee Ann Garrett-Sinha and Shinu A. John and Sarah L. Gaffen},
  journal={Current Opinion in Rheumatology},
  year={2008},
  volume={20},
  pages={519–525}
}
Purpose of reviewSystemic lupus erythematosus etiology includes both genetic and environmental factors. Evidence suggests that many genetic loci in humans and mouse models contribute to the occurrence and clinical presentation of lupus. This large array of different genes affects many aspects of immune cell function, including the activation and functional differentiation of B cells, T cells, dendritic cells and other immune cells. In particular, the T-cell components that contribute to… 
IL-17 in B Cell Biology and Systemic Lupus Erythematosus
TLDR
The hypothesis that IL-17 might play a pivotal role in the pathophysiology of auto-immune diseases such as SLE because of its combined actions on both T cell driven inflammation and B cell biology is proposed and discussed.
Th17 cells and CD4(+) multifunctional T cells in patients with systemic lupus erythematosus.
TLDR
Taken together, data indicate the participation of recently activated Th17 cells and MTF cells in the SLE pathophysiology.
Disturbed T Cell Signaling and Altered Th17 and Regulatory T Cell Subsets in the Pathogenesis of Systemic Lupus Erythematosus
TLDR
The literature is summarized that addresses the roles of T cell signaling, Th17 and regulatory T cells (Tregs) in the development of SLE, and increased numbers of autoreactive Th 17 cells have been documented, and Th17 cells appear to be responsible for tissue inflammation and damage.
Interleukin‐17 and systemic lupus erythematosus: current concepts
TLDR
The work that has explored the development and behaviour of IL‐ 17‐producing cells in SLE is discussed, and different mechanisms by which IL‐17 could potentially augment inflammation and autoantibody production in the context of SLE are proposed.
Recovery of the immune balance between Th17 and regulatory T cells as a treatment for systemic lupus erythematosus.
TLDR
It is hypothesized that for the treatment of SLE, therapeutic agents should focus on therapeutic agents that can regulate the immune balance between Th17 and Treg cells rather than on those that exclusively regulate Th17 cells.
Th17 cells in rheumatoid arthritis and systemic lupus erythematosus
  • A. Pernis
  • Medicine
    Journal of internal medicine
  • 2009
TLDR
This review will discuss recent studies that have begun elucidating the factors that regulate the development of Th17 cells and provide a brief overview of the role of Th 17 cells in RA and SLE.
Cellular and molecular pathogenesis of systemic lupus erythematosus: lessons from animal models
TLDR
The present understanding is reviewed - as garnered from studying mouse models - about the roles of various immune cells in lupus pathogenesis about the appearance of autoantibodies against nuclear antigens and the involvement of multiple organ systems, including the kidneys.
Immunoregulation therapy changes the frequency of interleukin (IL)‐22+CD4+ T cells in systemic lupus erythematosus patients
TLDR
Results suggest that elevated IL‐22 is correlated withIL‐22+CD4+T cells, especially Th22 cells, and may have a co‐operative or synergetic function in the immunopathogenesis of SLE, thus providing new insights into the mechanism of GC, CYC and HCQ in the treatment of Sle.
The potential role of Th17 cells and Th17-related cytokines in the pathogenesis of lupus nephritis
TLDR
The results suggest the potential role of the IL-23/Th17 axis in the intra-renal inflammation of SLE patients and positively correlated with renal SLEDAI and histological activity index for LN patients.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 71 REFERENCES
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
TLDR
Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.
Interleukin 17–producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice
TLDR
It is demonstrated that autoimmune BXD2 mice express more IL-17 and show spontaneous development of germinal centers (GCs) before they increase production of pathogenic autoantibodies, suggesting a mechanism by which IL- 17 drives autoimmune responses by promoting the formation of spontaneous GCs.
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
TLDR
In vivo, antibody to IL- 17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused Chemokine production and leukocyte infiltration, indicating a unique T helper lineage that regulates tissue inflammation.
Interleukin 27 negatively regulates the development of interleukin 17–producing T helper cells during chronic inflammation of the central nervous system
TLDR
It is shown that IL-27 receptor–deficient mice chronically infected with Toxoplasma gondii developed severe neuroinflammation that was CD4+ T cell dependent and was associated with a prominent IL-17 response.
Increased interleukin-17 production in patients with systemic sclerosis.
TLDR
IL-17 overproduction plays an important role in the pathogenesis of SSc, especially in the early stages of the disease, by inducing the proliferation of fibroblasts and the production of IL-1 and the expression of adhesion molecules on endothelial cells.
A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage
TLDR
The evolution of the understanding of the TH17 pathway illuminates a shift in immunologists' perspectives regarding the basis of tissue damage, where for over 20 years the role of TH1 cells was considered paramount.
Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17*
TLDR
Evidence is presented that murine IL-23, which is produced by activated dendritic cells, acts on memory T cells, resulting in elevated IL-17 secretion, which suggests that during a secondary immune response, IL- 23 can promote an activation state with features distinct from the well characterized Th1 and Th2 profiles.
Ets-1 is a negative regulator of Th17 differentiation
TLDR
It is reported that Ets-1 is a negative regulator of Th17 differentiation, and plays a role in the clearance of extracellular bacteria and increased mucus production by airway epithelial cells in an IL-17–dependent manner.
The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation.
TLDR
With this paradigm shift in understanding of autoimmune inflammation pathogenesis comes exciting opportunities to identify and to target therapeutically molecules within the IL-23/Th(17) axis that are key to disease development.
IL-17 family cytokines and the expanding diversity of effector T cell lineages.
TLDR
The factors that specify differentiation of a new effector T cell lineage-Th17-have now been identified, providing a new arm of adaptive immunity and presenting a unifying model that can explain many heretofore confusing aspects of immune regulation, immune pathogenesis, and host defense.
...
1
2
3
4
5
...