1,721,357 research outputs found
Corrigendum to “Tregs and Th17 lymphocytes in human DYRK1A haploinsufficiency” [Immunol. Lett. 214 (2019) 52–54](S0165247819302342)(10.1016/j.imlet.2019.08.003)
No full textThe authors regret for not publishing the correct order of authors in the original article. The correct authorship is: Valencic E, Todaro F, Piscianz E, Sirchia F, Spinelli AM, Tommasini A, Badolato R, Faletra F. The authors apologise for the inconvenience caused
Sequele post-acute da SARS-CoV-2 (PASC): ovvero il lungo inverno del Covid-19
No full textAncora una volta, partiamo dalla Storia. Da quella della pandemia che più spesso abbiamo confrontato a questa attuale, partiamo cioè dall’influenza Spagnol
Patient-centred screening for primary immunodeficiency, a multi-stage diagnostic protocol designed for non-immunologists: 2011 update
No full textCOVID-19 and immune response: Weak defences and self-harms,Covid-19 e risposta immune: Tra debolezze in difesa ed errori in attacco
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Selective IgA deficiency: ruling out coeliac disease and selective antibody deficiency to polysaccharides
No full textGenetics of inflammatory bowel disease from multifactorial to monogenic forms
Full text linkInflammatory bowel disease (IBD) is a group of chronic multifactorial disorders. According to a recent study, the number of IBD association loci is increased to 201, of which 37 and 27 loci contribute specifically to the development of Crohn’s disease and ulcerative colitis respectively. Some IBD associated genes are involved in innate immunity, in the autophagy and in the inflammatory response such as NOD2, ATG16L1 and IL23R, while other are implicated in immune mediated disease (STAT3) and in susceptibility to mycobacterium infection (IL12B). In case of early onset of IBD (VEO-IBD) within the 6th year of age, the disease may be caused by mutations in genes responsible for severe monogenic disorders such as the primary immunodeficiency diseases. In this review we discuss how these monogenic disorders through different immune mechanisms can similarly be responsible of VEO-IBD phenotype. Moreover we would highlight how the identification of pathogenic genes by Next Generation Sequencing technologies can allow to obtain a rapid diagnosis and to apply specific therapies
The MDM2 inhibitor Nutlin-3 modulates dendritic cell-induced T cell proliferation
No full textNutlin-3, a small molecule inhibitor of the MDM2/p53 interaction, has been recently taken into consideration as a promising therapeutic tool for tumor treatment based on its ability to stabilize and activate the p53 transcription factor pathway. Since Nutlin-3 displays non cell-autonomous tumor-suppressor activities, we wanted to investigate its effect on dendritic cell functions, given the central role of these cells in the modulation of the immune response. We found that Nutlin-3 alone slightly affected the levels of major histocompatibility complex and costimulatory molecules and significantly promoted the ability of dendritic cells to stimulate T cells in the mixed lymphocyte reaction. Taken together, our findings suggest that the ability of Nutlin-3 to modulate dendritic cell functions and therefore lymphocyte proliferation might represent an additional important mechanism by which Nutlin-3 exerts its non cell-autonomous tumor-suppression function. © 2012 American Society for Histocompatibility and Immunogenetics
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