Interleukin‐23: as a drug target for autoimmune inflammatory diseases

Tang, Chun-Lei; Chen, Shu; Qian, Hai; Huang, Wenlong

doi:10.1111/j.1365-2567.2011.03522.x

Cited by 281 publications

(217 citation statements)

References 109 publications

(212 reference statements)

Supporting

Mentioning

208

Contrasting

Unclassified

Order By: Relevance

“…However, when these psoriatic patients received fumaric acid esters therapy, the level was decreased but this may be due to the effect of treatment [15]. IL-23 has the ability to enhance the expansion of T helper type 17 (Th17) cells indicating the responsibility for many of the inflammatory autoimmune responses [16]. In this study, IL-12 and IL-23 were significantly increased in all cases of psoriasis than controls.…”

Section: Discussionmentioning

confidence: 63%

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

et al. 2013

View full text Add to dashboard Cite

Abstract.To evaluate the role of psoriasin, koebnerisin, interleukn (IL)-12 and IL-23 in the pathogenesis of psoriasis and their relations to Psoriasis Area Severity Index (PASI) and obesity. Thirty patients had chronic plaque psoriasis and 30 healthy subjects matched in age and sex were enrolled in this study. Serum from all subjects were used for determination of psoriasin, koebnerisin, IL-12 and IL-23 by ELISA kits. IL-23 and psoriasin were significantly higher in skin psoriasis compared to controls and psoriatic arthritis (PsA). There was a correlation between psoriasin and both PASI and obesity. On the other hand, IL-12 was significantly increased in PsA compared to skin psoriasis (p = 0.000) and controls. Its sensitivity and specificity were 87%, 93%; respectively. To our knowledge, psoriasin is the first biomarker confirm the link between obesity and psoriasis. The risk of developing psoriasis is directly related to higher BMI.

show abstract

Section: Discussionmentioning

confidence: 63%

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Thus anti-IL23 therapy could be a therapeutic target not only of inflammation but also bone erosion in RA. The level of interest in this target can be seen from the fact that 15 different IL23R antagonists are now reported to be in clinical or pre-clinical development [182] . Recent clinical studies associated with IL-23 inhibition in arthritis include the use of apilimod mesylate, an orally administered inhibitor of IL-12/IL-23 in RA [183] .…”

Section: Il-2 Superfamilymentioning

confidence: 99%

“…However, due to the common p40 subunit and IL12RB1 chain, the major drawback of anti-IL23 treatment may be the simultaneous inhibition of IL-12 and a possible shutdown of the immune system. Nevertheless, it would be much more useful to design drugs that target the IL23p19 or IL23RA itself, thus inhibiting IL-23 without modifying the effects of IL-12 (e.g., MP-196, FM-303, IL-23 Adnectin) [182] .…”

Section: Il-2 Superfamilymentioning

confidence: 99%

Interleukins and interleukin receptors in rheumatoid arthritis: Research, diagnostics and clinical implications

Magyari

Várszegi

Kövesdi

et al. 2014

WJO

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is an autoimmune disease, resulting in a chronic, systemic inflammatory disorder. It may affect many tissues and organs, but it primarily affects the flexible joints. In clinical practice patient care generates many questions about diagnosis, prognosis, and treatment. It is challenging for health care specialists to keep up to date with the medical literature. This review summarizes the pathogenesis, the polymorphisms of interleukin and interleukin genes and the standard available and possible future immunologic targets for RA treatment. The identification of diseaseassociated interleukin and interleukin receptor genes can provide precious insight into the genetic variations prior to disease onset in order to identify the pathways important for RA pathogenesis. The knowledge of the complex genetic background may prove useful for developing novel therapies and making personalized medicine based on the individual's genetics.

show abstract

“…IL-23 is crucial for generating Th17 cells that do not produce IL-10 and instead develop an encephalitogenic phenotype (41,58). DCs are main producers of IL-23, and pharmacological inhibition of IL-23 production or its neutralization is not only effective in experimental mouse models of EAE, but also in humans with Th17-dominated autoimmune diseases like psoriasis (36,(59)(60)(61). The mechanism underlying SFN-mediated IL-23 suppression through the direct Nrf2 activator SFN was one central question of our study.…”

Section: Sfn Treatment Inhibits Il23a/il12b Expression and Th17/th1 Dmentioning

confidence: 99%

Sulforaphane Protects from T Cell–Mediated Autoimmune Disease by Inhibition of IL-23 and IL-12 in Dendritic Cells

Geisel

Brück

Glocova

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

Sulforaphane (SFN), an isothiocyanate, is part of an important group of naturally occurring small molecules with anti-inflammatory properties. The published reports are best conceivable with an inhibition of T cell function, but the mode of action remains unknown. We therefore analyzed the effect of SFN on T cell–mediated autoimmune disease. Feeding mice with SFN protected from severe experimental autoimmune encephalomyelitis. Disease amelioration was associated with reduced IL-17 and IFN-γ expression in draining lymph nodes. In vitro, SFN treatment of T cells did not directly alter T cell cytokine secretion. In contrast, SFN treatment of dendritic cells (DCs) inhibited TLR4-induced IL-12 and IL-23 production, and severely suppressed Th1 and Th17 development of T cells primed by SFN-treated DCs. SFN regulated the activity of the TLR4-induced transcription factor NF-κB, without affecting the degradation of its inhibitor IκB-α. Instead, SFN treatment of DCs resulted in strong expression of the stress response protein heme oxygenase-1 (HO-1), which interacts with and thereby inhibits NF-κB p65. Consistent with these findings, HO-1 bound to p65 and subsequently inhibited the p65 activity at the IL23a and IL12b promoters. Importantly, SFN suppressed Il23a and Il12b expression in vivo and silenced Th17/Th1 responses within the CNS. Thus, our data show that SFN improves Th17/Th1-mediated autoimmune disease by inducing HO-1 and inhibiting NF-κB p65-regulated IL-23 and IL-12 expression.

show abstract

Interleukin‐23: as a drug target for autoimmune inflammatory diseases

Cited by 281 publications

References 109 publications

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

Interleukins and interleukin receptors in rheumatoid arthritis: Research, diagnostics and clinical implications

Sulforaphane Protects from T Cell–Mediated Autoimmune Disease by Inhibition of IL-23 and IL-12 in Dendritic Cells

Contact Info

Product

Resources

About