Ivana Marventano

Don Carlo Gnocchi Foundation

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Marina Saresella

Don Carlo Gnocchi Foundation

Mario Clerici

University of Milan

Federica Piancone

University of Foggia

Francesca La Rosa

Don Carlo Gnocchi Foundation

Domenico Caputo

Sapienza University of Rome

Marco Rovaris

Don Carlo Gnocchi Foundation

Raffaello Nemni

Don Carlo Gnocchi Foundation

Laura Mendozzi

Don Carlo Gnocchi Foundation

Franca Rosa Guerini

Don Carlo Gnocchi Foundation

Ambra Hernis

Don Carlo Gnocchi Foundation

Cooperative Institutions

University of Milan

108

Istituti di Ricovero e Cura a Carattere Scientifico

Don Carlo Gnocchi Foundation

Charité - Universitätsmedizin Berlin

German Rheumatism Research Centre

Leibniz Association

Humboldt-Universität zu Berlin

Freie Universität Berlin

Institute of Immunology

Inserm

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Myelin basic protein-specific T lymphocytes proliferation and programmed cell death in demyelinating diseases

Clinical Immunology (2008)

Marina Saresella Ivana Marventano Franca Rosa Guerini Milena Zanzottera Serena Delbue

Pathogenesis

10.1016/j.clim.2008.08.010

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Citations (15)

Costimulatory Pathways in Multiple Sclerosis: Distinctive Expression of PD-1 and PD-L1 in Patients with Different Patterns of Disease

The Journal of Immunology (2009)

Daria Trabattoni Marina Saresella Michela Pacei Ivana Marventano Laura Mendozzi

T lymphocytes costimulatory molecules, including CD80, CD86, CD28, CTLA4, PD-1, PD-L1, and B7-H3, are associated with the preferential production of pro- or anti-inflammatory cytokines. We analyzed the expression of these molecules and myelin basic protein (MBP)-specific IL-10 and IFN-gamma production in patients with multiple sclerosis (MS) with relapsing-remitting acute (AMS, n = 40) or stable (SMS, n = 38). Twenty-two patients successfully undergoing therapy with glatimer acetate (n = 12) or IFNbeta (n = 10) were also analyzed. MBP-specific and PD-1-expressing T lymphocytes, PD-L1-expressing CD19(+) cells, and PD-L1(+)/IL-10(+)/CD14(+) and CD19(+) cells were significantly augmented in SMS patients. Additionally, MBP-specific and annexin V-expressing CD4(+) and CD8(+) (apoptotic) T lymphocytes were augmented and pAkt-positive (proliferating) cells were decreased in SMS compared with AMS patients. PD-1 ligation resulted in the increase of pAkt(+) lymphocytes in AMS patients alone. B7-H3 expression and IFN-gamma production were comparable in all individuals but the PD-L1(+)/IL-10(+) over B7-H3(+)/IFN-gamma(+) ratio was significantly lower in AMS compared with SMS patients. Finally, PD-L1 expression on immune cells was reduced in treated patients, suggesting that therapy-induced disease remission is not associated with the modulation of the expression of this molecule. The PD-1/PD-L1 pathway plays an important role in modulating immune functions in MS patients; monitoring and targeting these proteins could offer diagnostic and therapeutic advantages.

CD80

CD86

10.4049/jimmunol.0901038

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Citations (85)

Stavudine Reduces NLRP3 Inflammasome Activation and Upregulates Aβ-Autophagy

bioRxiv (Cold Spring Harbor Laboratory) (2018)

Francesca La Rosa Marina Saresella Ivana Marventano Federica Piancone Enrico Ripamonti

Abstract Alzheimer’s disease (AD) is associated with amyloid-beta (Aβ) deposition and neuroinflammation, possibly driven by activation of the NLRP3 inflammasome. Nucleoside reverse transcriptase inhibitors (NRTI) hamper the assembly of the NLRP3 inflammasome; we analyzed whether stavudine (D4T), a prototypical NRTI, modulates Aβ-mediated inflammasome activation; because neuroinflammation impairs Aβ clearance by phagocytes, phagocytosis and autophagy were examined as well. THP-1-derived macrophages were stimulated in vitro with Aβ 42 alone or after LPS priming with/without D4T. NLRP3 and TREM2 expression was analyzed by RT-PCR, phagocytosis and ASC-Speck by AmnisFlowSight, NLRP3-produced cytokines by ELISA, authophagy by P-ELISA evaluation of P-ERK and P-AKT. Results showed that IL1β, IL18 and caspase-1 were increased whereas Aβ-phagocytosis and TREM2 were reduced in LPS+Aβ 42 -stimulated cells. D4T reduced NLRP3 assembly as well as IL18 and caspase-1 production, but not IL1β, phagocytosis, and TREM2. P-AKT expression was augmented and P-ERK was reduced by D4T, suggesting a stimulatory effect on autophagy. D4T reduces NLRP3 inflammasome-associated inflammation, possibly restoring autophagy, in an in vitro model of AD; it will be interesting to verify its possibly beneficial effects in the clinical scenario.

TREM2

AIM2

10.1101/377945

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Citations (2)

Hypoxia modulates the effect of dihydroartemisinin on endothelial cells

Biochemical Pharmacology (2011)

Sarah D’Alessandro Nicoletta Basilico Yolanda Corbett Diletta Scaccabarozzi Fausta Omodeo‐Salè

Dihydroartemisinin

Hypoxia

10.1016/j.bcp.2011.06.002

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Citations (31)

Vitamin D receptor (VDR) gene SNPs influence VDR expression and modulate protection from multiple sclerosis in HLA-DRB1*15-positive individuals

Brain Behavior and Immunity (2011)

Cristina Agliardi Franca Rosa Guerini Marina Saresella Domenico Caputo Maurizio Leone

10.1016/j.bbi.2011.05.015

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Citations (74)

JC virus detection and JC virus-specific immunity in natalizumab-treated Multiple Sclerosis patients

Journal of Translational Medicine (2012)

Roberta Mancuso Marina Saresella Ambra Hernis Ivana Marventano Cristian Ricci

The use of natalizumab in multiple sclerosis (MS) may favour JC virus reactivation; this phenomenon is usually asymptomatic but can, albeit rarely, evolve into frank progressive multifocal leucoencephalopathy (PML).JCV-specific CD8+ T lymphocytes were evaluated by flow cytometry over a 24-month period in 24 natalizumab-treated MS patients in whom JCV DNA was or was not detected in blood using quantitative real-time polymerase chain reaction; all these cases were asymptomatic.Perforin- and grazymes-containing VP-1-specific CD8+ T lymphocytes were reduced whereas CD107a-expressing cells were increased in JCV positive patients, suggesting an active degranulation of these cells; naïve CD8+ T lymphocytes were also decreased whereas memory cells were increased in patients in whom JCV reactivation was observed.The presence of a CD8+ T lymphocyte-mediated effector immune response offers a greater insight into reactivation of JCV and its clinical sequelae, and may help the monitoring of patients on natalizumab therapy.

Natalizumab

JC Virus

10.1186/1479-5876-10-248

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Citations (20)

PD1 Negative and PD1 Positive CD4+ T Regulatory Cells in Mild Cognitive Impairment and Alzheimer's Disease

Journal of Alzheimer s Disease (2010)

Marina Saresella Elena Calabrese Ivana Marventano Federica Piancone Andrea Gatti

Regulatory T lymphocytes (Treg) play a fundamental importance in modulating the relative balance between inflammation and immune tolerance, and alterations of these cells are observed in inflammatory diseases. To better characterize the neuroinflammatory processes suggested to be associated with Alzheimer's disease (AD) and to clarify the possible role of Treg cells in this process, we extensively analyzed these cells (CD4 + CD25highFoxp3+) in patients with either severe AD (n=25) or mild cognitive impairment (MCI) (n=25), comparing the results with those of two groups of healthy controls (HC) (n=55). Because the intra- or extracellular expression of programmed death receptor 1 (PD1) identifies functionally diverse subsets of Treg we also analyzed such subpopulations. Results showed that, whereas both Treg and PD1pos Treg are increased in MCI and AD patients compared to HC, PD1neg Treg, the subpopulation of Treg cells endowed with the strongest suppressive ability, are significantly augmented in MCI patients alone. In these patients amyloid-β-stimulated-T cells proliferation was reduced and Treg-mediated suppression was more efficient compared to both AD and HC. The observation that PD1neg Treg, cells are increased in MCI patients reinforces the inflammatory origin of AD and supports a possible beneficial role of these cells in MCI that is lost in patients with full-blown AD.

Cognitive Decline

Immune Dysregulation

Treg cell

10.3233/jad-2010-091696

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Citations (134)

Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

European Journal of Immunology (2019)

Andrea Cossarizza Hyun‐Dong Chang Andreas Radbruch Andreas Acs Dieter Adam

These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.

Mass cytometry

Cytometry

10.1002/eji.201970107

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Citations (866)

Pharmacological and Epigenetic Regulators of NLRP3 Inflammasome Activation in Alzheimer’s Disease

Pharmaceuticals (2021)

Francesca La Rosa Roberta Mancuso Simone Agostini Federica Piancone Ivana Marventano

Activation of the NLRP3 inflammasome complex results in the production of IL-18, Caspase-1 and IL-1β. These cytokines have a beneficial role in promoting inflammation, but an excessive activation of the inflammasome and the consequent constitutive inflammatory status is a negative factor in human pathologies including Alzheimer's Disease (AD). MicroRNAs (miR-NAs) target the 3'UTR region of NLRP3, preventing the activation of the inflammasome and inhibiting cytokine production. Because Stavudine (D4T), an antiretroviral drug, was recently shown to reduce inflammasome activation, we verified whether its effect is mediated by miR-7-5p, miR-22-3p, miR-30e-5p and miR-223-3p: miRNAs that bind the NLRP3-mRNA-UTR region and interfere with protein translation, reducing NLRP3 activation. Peripheral blood mononuclear cells (PBMCs) of twenty AD patients and ten sex-matched Healthy Controls (HC) were stimulated with Lipopolysaccharides (LPS)+Amyloid-beta (Aβ42) in the absence/presence of D4T. Expression of genes within the inflammasome complex and of miRNAs was evaluated by RT-PCR; cytokines and caspase-1 production was measured by ELISA. Results have shown that: NLRP3, ASC, IL-1β and IL-18 expression, as well as IL-18, IL-1β and caspase-1 production, were significantly augmented (p < 0.05) in LPS+Aβ42-stimulated PBMCs of AD patients compared to HC. D4T reduced the expression of inflammasome genes and cytokine production (p < 0.005). miR-7-5p and miR-223-3p expression was significantly increased in LPS+Aβ42-stimulated PBMCs of AD patients (p < 0.05), and it was reduced by D4T in AD alone. In conclusion: miR-223-3p and mir-7-5p expression is increased in AD, but this does not result in down-regulation of NLRP3 inflammasome expression and of IL-1β and IL-18 production. D4T increased miRNA expression in HC but had an opposite effect in AD, suggesting that miRNA regulatory mechanisms are altered in AD.

AIM2

10.3390/ph14111187

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Citations (19)

The NLRP3 and NLRP1 inflammasomes are activated in Alzheimer’s disease

Molecular Neurodegeneration (2016)

Marina Saresella Francesca La Rosa Federica Piancone Martina Zoppis Ivana Marventano

Interleukin-1 beta (IL-1β) and its key regulator, the inflammasome, are suspected to play a role in the neuroinflammation observed in Alzheimer's disease (AD); no conclusive data are nevertheless available in AD patients. mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1β, IL-18) was up-regulated in severe and MILD AD. Monocytes co-expressing NLRP3 with caspase 1 or caspase 8 were significantly increased in severe AD alone, whereas those co-expressing NLRP1 and NLRP3 with PYCARD were augmented in both severe and MILD AD. Activation of the NLRP1 and NLRP3 inflammasomes in AD was confirmed by confocal microscopy proteins co-localization and by the significantly higher amounts of the pro-inflammatory cytokines IL-1β and IL-18 being produced by monocytes. In MCI, the expression of NLRP3, but not the one of PYCARD or caspase 1 was increased, indicating that functional inflammasomes are not assembled in these individuals: this was confirmed by lack of co-localization and of proinflammatory cytokines production. The activation of at least two different inflammasome complexes explains AD-associated neuroinflammation. Strategies targeting inflammasome activation could be useful in the therapy of AD.

NLRP1

AIM2

Proinflammatory cytokine

Interleukin 18

NALP3

Pyrin domain

10.1186/s13024-016-0088-1

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Citations (403)