Psoriatic disease treatment nowadays: unmet needs among the “jungle of biologic drugs and small molecules” (original) (raw)
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Recent Advances in Psoriasis Therapy: Trends and Future Prospects
Bentham Science Publishers, 2021
Background: Psoriasis is a challenging skin disorder due to its chronicity, high rate of prevalence, disability, comorbidity and disfiguration. It is a multi-system disorder that includes joints and metabolic syndromes. Psoriasis is a condition of pathologic interaction among immune cells, biological signaling molecules and skin cells. Several contributing factors are responsible for the exacerbation and onset of psoriasis, i.e. genetic factors and environmental factors such as medications, infectious diseases and lifestyle. Objectives: To study the new insights in the treatment of psoriasis and future prospects. Methods: This review article gives an insight on the current concepts of psoriasis and deals with discussing the initiation and development of the diseases. We described the pathogenetic pathway for psoriasis. The article focuses on the treatment approaches for psoriasis that have arisen from the dissection of the inflammatory psoriatic pathways. Results: We aimed to highlight the novel therapies and drugs used in the treatment of psoriasis, including food and drug administration (FDA) approved drugs and drugs under clinical trials. The treatment can be initiated for mild to the moderate diseased condition employing vitamin D3 analogues, corticosteroids and a combination of products as first-line therapy. Conclusion: Psoriasis can be managed by a proper understanding of the immune function. We have also discussed medicinal herbs used for psoriasis based on their ethnopharmacological knowledge and reported work of researchers.
Advances in Treatment Options for Psoriasis
Psoriasis is a skin disease that is evidenced primarily by plaques which can be seen throughout the body. Genetic predisposition that combines with an environmental trigger of the immune system is believed to be the root cause of psoriasis. This leads to signaling factors which coordinate the progression of inflammation and psoriatic plaques. Psoriatic patients commonly use topical agents, phototherapy, and systemic agents; however, biological therapies have become increasingly popular. This is primarily due to recent advances in the study of psoriasis which have shown that monoclonal antibodies and dimeric fusion proteins inhibit key signaling molecules within the inflammatory cascade such as TNFa, IL-12 and IL-23. This article reviews the advances made to understand the role of TNFa in the progression of psoriasis, discusses treatment options such as topical agents, phototherapy and systemic agents, and then compares a variety of monoclonal antibodies and dimeric fusion proteins as biological therapies. penetrate the lymphatic system, activate T cells, and engender the secretion of cytokines which induce the inflammatory cascade and psoriatic skin plaques . However, in the innate immune system there are more identifiable mediators. For instance, toll-like receptors (TLRs) which are type 1 membrane glycoproteins that recognize pathogen associated molecular patterns (PAMPs), are important in the inflammatory cascade . Within this cascade the keratinocyte barrier can be disturbed, NK lymphocytes can be activated, and natural killer receptors can be expressed. Interferon gamma (IFNγ), released by NK lymphocytes, and TNFα, released by keratinocytes, work together to create inflammation, which is a physical characteristic of plaque psoriasis . Another prevalent characteristic of plaque psoriasis is epidermal hyperplasia. Within this condition, keratinocytes proliferate and within the focal regions Type 1 effectors accumulate and induce cytokines such as IFNγ, and TNFα [16,. Specifically, IL-12 and IL-23 are related to T cell differentiation and activation of T helper 1 cells phenotypes.
Biomedicines, 2021
Psoriasis is an immune-mediated inflammatory disease, with a chronic relapsing-remitting course, which affects 2–3% of the worldwide population. The progressive acquisitions of the inflammatory pathways involved in the development of psoriasis have led to the identification of the key molecules of the psoriatic inflammatory cascade. At the same time, psoriasis therapy has radically evolved with the introduction of target molecules able to modify the natural history of the disease, acting specifically on these inflammatory pathways. For these reasons, biologics have been demonstrated to be drugs able to change the disease’s natural history, as they reduce the inflammatory background to avoid irreversible organ damage and prevent systemic complications. However, several issues related to the use of biologics in patients with systemic comorbidities, remain open. All these data reflect the extraordinary potentiality of biologics, but also the unmet medical need to improve our knowledge ...
Old and New Biological Therapies for Psoriasis
International journal of molecular sciences, 2017
Biological therapy became available for psoriasis with the introduction of alefacept at the beginning of this century. Up to then, systemic treatment options comprised small molecule drugs, targeting the immune system in a non-specific manner. The first biologics targeted T-cell activation and migration and served as an alternative to small molecules. However, significant improvement in outcome was first accomplished with the introduction of tumor necrosis factor-α inhibitors that were already approved for other inflammatory disorders, including rheumatic diseases. Along with the progress in understanding psoriasis pathogenesis, highly targeted and effective therapies have since developed with the perspective not only to improve but to clear psoriasis. These accomplishments enable future achievement of advanced goals to individualize treatment best suited for each patient. Mechanistic studies with patients treated with the new highly targeted biologics may guide us towards these goa...
Biologics for psoriasis: What is new?
Dermatologic Therapy, 2019
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Psoriasis: from basic and clinical research to the development of new treatments
Gaceta de M�xico
Psoriasis is an incurable cutaneous disease that affects 2.9% of the Mexican population, and it is therefore important for the impact of translational medicine on the development of anti-psoriatic drugs to be analyzed. In this review, current etiopathogenic concepts of the disease are discussed, and articles on drugs under development published between 2005 and 2017 are reviewed; in addition, a critical analysis on future perspectives for the development new treatments is presented. The use of translational medicine bi-directional strategies of has allowed to significantly increase the number of available anti-psoriatic therapies. Eighteen new investigational drugs were found. Characterization of antigens responsible for immune activation, identification of predictive biomarkers with pharmacologic efficacy, and the development of more representative disease models, as well as the integration of pharmacogenomic aspects to translational medicine strategies were identified as relevant aspects that should be incorporated in the development of new therapeutic options.
Future Perspectives in the Treatment of Psoriasis
Management of Psoriasis, 2009
All available antipsoriatic therapies are of symptomatic character. Treatments established so far are limited in their use due to side effects or lack of efficacy resulting in poor quality of life for affected people. Development of new therapeutic approaches would not only broaden our armamentarium against psoriasis, but could also increase our understanding of the pathogenesis of this disease. In brief, 2 main targets represent attractive candidates, either the keratinocyte itself or the immune system. Promising therapeutic strategies include: (1) the search for new psoriasis susceptibility genes and their resulting phenotypes; (2) the interference with certain parts of cell signaling pathways that are involved in inflammatory processes; (3) the inhibition or elimination of activated T lymphocytes, e.g. by blocking of costimulatory signals or by deviation of a pathogenic immune response into a nonpathogenic one; (4) the blockade of proinflammatory cytokines; (5) the inhibition of leukocyte extravasation or trafficking; (6) the inhibition of angiogenesis. Some of these strategies are in phase 2 trials, others have already reached phase 3 status and are close to being approved by medicine agencies, and some are still visions of the future. This book chapter will give an overview of these new treatment strategies.
[Psoriasis: pathogenesis and treatment]
Revue médicale de Bruxelles, 2003
Psoriasis is a T-cell mediated disease. Its pathogenesis is linked to the activation of T-cells by antigen-presenting cells and secretion of cytokines able to modulate keratinocyte proliferation and differentiation. Antigens involved in psoriasis triggering are unidentified. Several new biological immunomodulatory treatments able to block T-cell activation and epidermal cells modifications are currently investigated.
Autoimmunity Reviews, 2014
Psoriatic Arthritis (PsA) is a chronic inflammatory arthropathy associated with psoriasis. Psoriasis (PsO) is a chronic, inflammatory skin disease, characterized by hyperproliferation and aberrant differentiation of keratinocytes. PsA and PsO can be considered as a unique disease and are immune-mediated diseases and both innate and adaptive immunity play a role in their pathogenesis. Initially, PsO and PsA were thought to be Th1-mediated diseases, however, in the last years, several studies have shown the role of interleukin 17 (IL-17) and Th17 cells in the pathogenesis of PsA and PsO. Th17 cells have been detected in dermal infiltrates of psoriatic lesions as well as in synovial fluid. Interleukin (IL)-23, produced by antigen presenting cells (APC), especially by dendritic cells (DC), is the key regulator cytokine for Th17 and IL-17 production. In this review we discuss the role of IL-17 and IL-23 in the pathogenesis of PsO and PsA and their role as therapeutic targets for PsO and PsA treatment.