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עמוד בית
Thu, 30.07.26

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February 2024
Sotirios G. Tsiogkas MD, Yoad M. Dvir, Yehuda Shoenfeld MD FRCP MaACR, Dimitrios P. Bogdanos MD PhD

Over the last decade the use of artificial intelligence (AI) has reformed academic research. While clinical diagnosis of psoriasis and psoriatic arthritis is largely straightforward, the determining factors of a clinical response to therapy, and specifically to biologic agents, have not yet been found. AI may meaningfully impact attempts to unravel the prognostic factors that affect response to therapy, assist experimental techniques being used to investigate immune cell populations, examine whether these populations are associated with treatment responses, and incorporate immunophenotype data in prediction models. The aim of this mini review was to present the current state of the AI-mediated attempts in the field. We executed a Medline search in October 2023. Selection and presentation of studies were conducted following the principles of a narrative–review design. We present data regarding the impact AI can have on the management of psoriatic disease by predicting responses utilizing clinical or biological parameters. We also reviewed the ways AI has been implemented to assist development of models that revolutionize the investigation of peripheral immune cell subsets that can be used as biomarkers of response to biologic treatment. Last, we discussed future perspectives and ethical considerations regarding the use of machine learning models in the management of immune-mediated diseases.

April 2019
Lazaros I. Sakkas MD PhD, Dimitrios P. Bogdanos MD PhD, Dimitrios Boumpas MD, Zisis Mamouris PhD, Athanasios Gkoutzourelas MD, Athanasios Mavropoulos PhD, Zisis Tsouris PhD, Stamatis-Nickοlaos Liossis MD, Dimitrios Daoussis MD, Dimitrios Vasilopoulos MD, Maria Tektonidou MD, Athanasios Tzioufas MD, George Efthymiou BSc, Efthymios Dardiotis MD, George Kitas MD PhD, Κassem Sharif MD, Miri Blank MD, Dimitrios Karussis MD, Doron Rimar MD, Gleb Slobodin MD, Bat-Sheva Porat-Katz MD, Zahava Vadasz MD PhD, Howard Amital MD MHA, Elias Toubi MD and Yehuda Shoenfeld MD FRCP MaACR
September 2016
Lazaros I. Sakkas MD DM PhD (London) FRCP (London) and Dimitrios P Bogdanos MD PhD (London)

Systemic sclerosis (SSc) is characterized by extensive collagen deposition, microvasculopathy and autoantibodies. All three features can be promoted by activation of T cells and B cells. T cells are of Th2 type producing profibrotic cytokines IL-4 and IL-13 and inducing dendritic cell maturation that promotes Th2 response. B cells are overactivated and promote fibrosis by autoantibodies that activate fibroblasts or inhibit the degradation of extracellular matrix. They also promote fibrosis by cell-cell contact with fibroblasts or dendritic cells. B cells, through autoantibodies, may promote vasoconstriction and obliterative vasculopathy. They may also sustain activation of T cells by functioning as antigen-presenting cells. An immunoregulatory subset of B cells, namely IL-10-producing Bregs, is decreased in SSc. Finally, B cells have a critical role in animal models of SSc. All this evidence suggests an important role for B cells in the pathogenesis of SSc and makes B cells a potential target for therapeutic intervention in this disease. 

 

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