Publications by authors named "G Dessole"

Advanced therapy medicinal products (ATMPs) are potential game changers in modern medical care with an anticipated major impact for patients and society. They are a new drug class often referred to as "living drugs," and are based on complex components such as vectors, cells and even tissues. The production of such ATMPs involves innovative biotechnological methods.

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This study is primarily aimed at assessing serum changes on a large panel of proteins in patients with chronic back pain following spa therapy, as well as evaluating different spa therapy regimens as a preliminary exploratory clinical study. Sixty-six patients with chronic back pain secondary to osteoarthritis were randomly enrolled and treated with daily mud packs and bicarbonate-alkaline mineral water baths, or a thermal hydrotherapy rehabilitation scheme, the combination of the two regimens or usual medication only (control group), for two weeks. Clinical variables were evaluated at baseline, after 2 and 12 weeks.

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Background: Ankylosing spondylitis (AS) is a complex chronic inflammatory disease strongly associated with the majority of human leucocyte antigen (HLA)-B27 alleles. HLA-E molecules are non-classical major histocompatibility complex (MHC) class I molecules that specifically interact with the natural killer receptors NKG2A (inhibitory) and NKG2C (activating), and have been recently proposed to be involved in AS pathogenesis.''.

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HLA-B27 (B27) interactions with the killer-cell immunoglobulin-like receptors (KIR) have been implicated in the pathogenesis of ankylosing spondylitis (AS), with consistent differences among populations. KIR3DL1 and possibly KIR3DS1 interact with classical B27, whereas KIR3DL2 binds B27 heavy chain dimers. The aim of this review is to summarize data from recent studies performed in our laboratory and from the literature, which provide support for a possible role of KIR3DL2/B27 dimer interactions in the pathogenesis of AS.

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Psoriatic arthritis (PsA) is a frequent chronic inflammatory disease characterized by joint and skin involvement, and by typical extra-articular manifestations. Although the pathogenesis of PsA is still under investigation, the available evidence suggests the importance of the patient's genetic background, microbial or environmental triggers, and an imbalance in the adaptive and acquired immune system, resulting in the production of inflammatory mediators. New therapeutic approaches have been proposed, among them the use of modulators of intracellular signals and gene transcription such as PDE4-inhibiting compounds, which are able to modulate the activity of transcription factors such as CREB and NF-κB and therefore the synthesis of inflammatory mediators, resulting in immunoregulation.

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