Ustekinumab for the treatment of psoriasis

Laws, Philip; Warren, Richard B

doi:10.1586/eci.11.4

Cited by 9 publications

(5 citation statements)

References 61 publications

(79 reference statements)

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“…The results of two recent clinical trials seem to have caused a paradigm shift in therapy development. Unexpectedly, treatment of relapsing/remitting MS (RRMS) patients using an antibody against human anti-IL12p40 aiming at the simultaneous inhibition of Th1 and Th17 T cell responses as demonstrated in psoriasis (Laws and Warren 2011), showed no detectable clinical benefit in RRMS (Segal et al 2008). On the other hand, treatment of a similar group of patients with monoclonal antibodies against human CD20, causing profound and long lasting depletion of B cells, caused rapid and sustained suppression of neurological symptoms (Barun and Bar-Or 2012).…”

Section: Introductionmentioning

confidence: 99%

Antibodies Against Human BLyS and APRIL Attenuate EAE Development in Marmoset Monkeys

Jagessar

Heijmans

Bauer

et al. 2012

J Neuroimmune Pharmacol

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B lymphocyte stimulator (BLyS, also indicated as BAFF (B-cell activating factor) and CD257), and A Proliferation Inducing Ligand (APRIL, CD256) are two members of the TNF superfamily with a central role in B cell survival. Antibodies against these factors have potential therapeutic relevance in autoimmune inflammatory disorders with a proven pathogenic contribution of B cells, such as multiple sclerosis (MS). In the current study we performed a multi-parameter efficacy comparison of monoclonal antibodies against human anti-BLyS and anti-APRIL in a common marmoset (Callithrix jacchus) model of experimental autoimmune encephalomyelitis (EAE). A MS-like disease was induced by immunization with recombinant human myelin/oligodendrocyte glycoprotein (rhMOG) in complete Freund’s adjuvant. The results show that the anti-BLyS and anti-APRIL antibody cause significant depletion of circulating CD20+ B cells, but a small subset of CD20 + CD40high B cells was not depleted. Induction of CD20+ B cell depletion from lymph nodes was only observed in the anti-BLyS treated monkeys. Both antibodies had a significant inhibitory effect on disease development, but all monkeys developed clinically evident EAE. Anti-BLyS treated monkeys were sacrificed with the same clinical signs as saline-treated monkeys, but nevertheless displayed significantly reduced spinal cord demyelination. This effect was not observed in the anti-APRIL treated monkeys. The two antibodies had a different effect on T cell subset activation and the profiles of ex vivo released cytokines. In conclusion, treatment with anti-BLyS and anti-APRIL delays the development of neurological disease in a relevant preclinical model of MS. The two mAbs achieve this effect via different mechanisms.

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Section: Introductionmentioning

confidence: 99%

Antibodies Against Human BLyS and APRIL Attenuate EAE Development in Marmoset Monkeys

Jagessar

Heijmans

Bauer

et al. 2012

J Neuroimmune Pharmacol

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“…Additionally, newly developed biological agents have been employed to treat moderate to severe psoriasis with body surface area (BSA) greater than 10% or psoriasis area and severity index (PASI) higher than 10 [ 3 ], including tumor necrosis factor α antagonists (etanercept, infliximab, etc. ), alefacept, efalizumab, and ustekinumab [ 4 ]. As for topical treatment that is mainly for mild or moderate psoriasis, it includes ointments (e.g., calcipotriol, calcineurin inhibitors, tretinoin, glucocorticoid), medicated bath with diastase or herbal extracts, and phototherapy.…”

Section: Introductionmentioning

confidence: 99%

A clinical review of phototherapy for psoriasis

2017

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Psoriasis is an autoimmune inflammatory skin disease. In the past several decades, phototherapy has been widely used to treat stable psoriatic lesions, including trunk, scalp, arms and legs, and partial nail psoriasis. A variety of light/lasers with different mechanisms of action have been developed for psoriasis including ultraviolet B (UVB), psoralen ultraviolet A (PUVA), pulsed dye laser (PDL), photodynamic therapy (PDT), intense pulsed light (IPL), light-emitting diodes (LED), and so on. Because light/laser each has specific therapeutic and adverse effects, it is important to adequately choose the sources and parameters in management of psoriasis with different pathogenic sites, severities, and duration of the disorder. This review aims at providing most updated clinic information to physicians about how to select light/laser sources and individual therapeutic regimens. To date, UV light is primarily for stable plaque psoriasis and PDL for topical psoriatic lesions with small area, both of which are safe and effective. On the other hand, PUVA has better curative effects than UVB for managing refractory psoriasis plaques, if its side effects can be better controlled. PDL provides optimal outcomes on nail psoriasis compared with other lasers. Although the trails of low-level light/laser therapy (LLLT) are still small, the near infrared (NIR) and visible red light with low energy show promise for treating psoriasis due to its strong penetration and encouraging photobiomodulation. IPL is rarely reported for psoriasis treatment, but PDT-IPL has been found to offer a moderate effect on nail psoriasis. In brief, various phototherapies have been used either in different combinations or as monotherapy. The modality has become a mainstay in the treatment of mild-to-moderate psoriasis without systemic adverse events in today’s clinical practice.

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“…The novel IL-23/Th17 axis has attracted much attention with the successful application of ustekinumab, a monoclonal antibody against IL-12 and IL-23, in psoriasis and PsA [47–49]. Some success was also reported with anti-IL-17A and anti-IL-22 agents in animal models of psoriasis [50].…”

Section: Introductionmentioning

confidence: 99%

The Role of p38 MAPK in the Aetiopathogenesis of Psoriasis and Psoriatic Arthritis

Mavropoulos

Rigopoulou

Liaskos

et al. 2013

Clinical and Developmental Immunology

104

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The pathogenetic mechanisms responsible for the induction of immune-mediated disorders, such as psoriasis, remain not well characterized. Molecular signaling pathways are not well described in psoriasis, as well as psoriatic arthritis, which is seen in up to 40% of patients with psoriasis. Signaling pathway defects have long been hypothesized to participate in the pathology of psoriasis, yet their implication in the altered psoriatic gene expression still remains unclear. Emerging data suggest a potential pathogenic role for mitogen activated protein kinases p38 (p38 MAPK) extracellular signal-regulated kinase 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) in the development of psoriasis. The data are still limited, though, for psoriatic arthritis. This review discusses the current data suggesting a crucial role for p38 MAPK in the pathogenesis of these disorders.

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Ustekinumab for the treatment of psoriasis

Cited by 9 publications

References 61 publications

Antibodies Against Human BLyS and APRIL Attenuate EAE Development in Marmoset Monkeys

Antibodies Against Human BLyS and APRIL Attenuate EAE Development in Marmoset Monkeys

A clinical review of phototherapy for psoriasis

The Role of p38 MAPK in the Aetiopathogenesis of Psoriasis and Psoriatic Arthritis

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