Upregulated IL-23 and IL-17 in Behçet patients with active uveitis.

@article{Chi2008UpregulatedIA,
  title={Upregulated IL-23 and IL-17 in Behçet patients with active uveitis.},
  author={Wei Chi and Xuefei Zhu and Peizeng Yang and Xiaoli Liu and Xiaomin Lin and Hong-yan Zhou and Xiang-kun Huang and Aize Kijlstra},
  journal={Investigative ophthalmology \& visual science},
  year={2008},
  volume={49 7},
  pages={
          3058-64
        }
}
PURPOSE Behçet disease (BD) is a systemic inflammatory disease presumably caused by an autoimmune response. The interleukin (IL)-23/IL-17 pathway has been demonstrated to be involved in the development and maintenance of certain inflammatory diseases. This study was designed to investigate the role of IL-23 and IL-17 in BD. METHODS IL-23p19 mRNA in peripheral blood mononuclear cells (PBMCs) was examined using RT-PCR. The levels of IL-23, IL-17, and IFN-gamma in sera or PBMCs were detected by… 

Figures from this paper

Decreased interleukin 27 expression is associated with active uveitis in Behçet’s disease

The results of the present study suggest that a decreased IL-27 expression is associated with disease activity in BD patients and Manipulation of IL- 27 may offer a new treatment modality for this disease.

Up-regulation of Th17 and related cytokines in Behçet's disease corresponding to disease activity.

The results of this study suggest that up-regulated IL-17 expression may be associated with clinical activity of Behçet's disease.

Increased Expression of IL-22 Is Associated with Disease Activity in Behcet’s Disease

IL-22 was associated with disease activity in BD and correlated with the presence of small vessel inflammation, suggesting that it may be involved in its pathogenesis.

IL-17A has an important role in the acute attacks of Behçet's disease.

The role of IL-17A in the activity and different organ involvements of the disease is investigated using ELISA and data indicates that neutrophil activity is increased in BD patients with active uveitis.

IFN-alpha blocks IL-17 production by peripheral blood mononuclear cells in Behcet's disease.

In vitro experiments showed that IFN-α could inhibit IL-17 expression and increased IL-10 production by PBMCs and CD4(+) T cells.

Correlation between IL-17A/F, IL-23, IL-35 and IL-12/-23 (p40) levels in peripheral blood lymphocyte cultures and disease activity in Behcet’s patients

Since IL-35 levels were lower in active Behcet’s patients compared to inactive patients and healthy controls, there may be a plasticity between Th17 and Treg cells according to the state of disease activity.

Th17-Inducing Conditions Lead to in vitro Activation of Both Th17 and Th1 Responses in Behcet’s Disease

The results suggest that under Th17-stimulating conditions, T cells express both IL-17 and IFN-γ in BD, which might be associated with the increased innate responses, early tissue neutrophil infiltrations and late adaptive immunity in BD.

Key role for IL-21 in experimental autoimmune uveitis

It is shown that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina, underscoring the need forIL-21 in the development of this disease and suggesting that blocking IL- 21/γc–signaling pathways may provide a means for controlling CNS auto-inflammatory diseases.

Elevated Serum Levels of Interleukin-17A in Uveitis Patients

Serum IL-17A levels are elevated in uveitis patients, particularly in active Uveitis, and this study concludes that T helper 17 cells (Th17) is the signature cytokine of Th17 cells.
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References

SHOWING 1-10 OF 28 REFERENCES

Cytokine profile in Behçet's disease patients

The results suggest that the microenvironment of CD4 + T cells in active Behçet's disease may induce the production of more cells committed to Th1 than in BD patients in remission and healthy controls.

Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation

The data presented here indicate that IL-23 is an essential promoter of end-stage joint autoimmune inflammation, whereas IL-12 paradoxically mediates protection from autoimmune inflammation.

Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17*

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.

Divergent cytokine production profile in Behçet's disease. Altered Th1/Th2 cell cytokine pattern.

The immune system in BD may be characterized by a divergent cytokine production profile of mixed Th1/Th2 (Th0) cell type; IFN-gamma is critical in modulating the IL-4, IL-10, and IL-12 cytokine network pathway in this disease.

IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6.

This study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not, and a critical target of IL- 23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-21 to produce the proinflammatory mediators IL-17 and IL-6.

Increased expression of interleukin 17 in inflammatory bowel disease

It is likely that IL-17 expression in IBD may be associated with altered immune and inflammatory responses in the intestinal mucosa and increased in patients with inflammatory bowel disease.

IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

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.

High Levels of IL-17 in Rheumatoid Arthritis Patients: IL-15 Triggers In Vitro IL-17 Production Via Cyclosporin A-Sensitive Mechanism1

The results suggest for the first time that IL-15 may represent a physiological trigger that via cyclosporin A and steroid sensitive pathways leads to the overproduction of IL-17 in the joints of rheumatoid arthritis patients.

IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2–dependent mechanisms with implications for psoriasis pathogenesis

Indirect intradermal administration of IL-23 in mouse skin initiates a tumor necrosis factor–dependent, but IL-17A–independent, cascade of events resulting in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis.