Institutes
Clinical neuroimmunology
The unit of Clinical neuroimmunology is currently active in both experimental and clinical neuroimmunology with the aim to have a mutual transfer of scientific questions and experimental data between patients and in vitro or in vivo experimental studies. The two most complex systems of living organisms are the nervous and immune system. Their interaction, their cross-talk, in health and disease is even more complex, and only partially understood. There is no doubt that gaining knowledge in this field holds promise to unravel the pathogenic mechanism of several diseases whose etiology is elusive, such as multiple sclerosis, but also classical neurodegenerative disorders, in which the inflammatory component may play expected (detrimental), but also unexpected (protective) roles.
Research activity
Clinical neuroimmunology Unit has pioneered the use of gene therapy tools to interrogate experimental models of multiple sclerosis, as a paradigm of a neuroimmunological disease. The group currently focuses attention on the relationship between adaptive and innate immune cells, classical immune mediators, and neuronal integrity, brain function, cognition.
The unit has described microglial microvesicles in the cerebrospinal fluid of neurological patients as a biomarker of microglia activation and therefore neuroinflammation. Researchers are currently investigating the biogenesis of glial microvesicles to characterize their role in the pathogenesis of inflammatory brain disorders, they are analyzing their cargo to propose more refined biomarkers able to identify microglia activation and phenotype, and they are exploring the use of microvesicles as drug delivery tools.
Eventually, this group is exploring the role of neuroinflammation in psychiatric diseases by assessing the peripheral blood immune profile of patients affected by schizophrenia, major depression, bipolar disorders. Clinical neuroimmunology unit is also involved in prospective studies on at risk populations, to understand if neuroinflammation might be a plausible therapeutic target for psychoses.
The unit has described microglial microvesicles in the cerebrospinal fluid of neurological patients as a biomarker of microglia activation and therefore neuroinflammation. Researchers are currently investigating the biogenesis of glial microvesicles to characterize their role in the pathogenesis of inflammatory brain disorders, they are analyzing their cargo to propose more refined biomarkers able to identify microglia activation and phenotype, and they are exploring the use of microvesicles as drug delivery tools.
Eventually, this group is exploring the role of neuroinflammation in psychiatric diseases by assessing the peripheral blood immune profile of patients affected by schizophrenia, major depression, bipolar disorders. Clinical neuroimmunology unit is also involved in prospective studies on at risk populations, to understand if neuroinflammation might be a plausible therapeutic target for psychoses.
Lecca D, Marangon D, Coppolino G, Menendez Mendez A, Finardi A, Dalla Costa G, Martinelli V, Furlan R, Abbracchio M. MiR-125a- 3p timely inhibits oligodendroglial maturation and is pathologically up-regulated in human multiple sclerosis. Scientific Reports 2016 6: 34503.
Casella G, Garzetti L, Gatta AT, Finardi A, Maiorino C, Ruffini F, Martino G, Muzio L, Furlan R. IL4 induces IL6 producing M2 macrophages associated to inhibition of neuroinflammation in vitro and in vivo. J Neuroinflamm. 2016 13:139.
Brambilla P, Bellani M, Isola M, Bergami A, Marinelli V, Dusi N, Rambaldelli G, Tansella M, Finardi AM, Martino G, Perlini C, Furlan R. Increased M1/decreased M2 signature and signs of Th1/Th2 shift in chronic patients with bipolar disorder, but not in those with schizophrenia. Transl Psychiatry. 2014 Jul 1;4:e406.
Agosta F, Dalla Libera D, Gioele Spinelli E, Finardi A, Canu E, Bergami A, Bocchio Chiavetto L, Baronio M, Comi G, Martino G, Matteoli M, Magnani G, Verderio C, Furlan R. Myeloid microvesicles in CSF are associated with myelin damage and neuronal loss in mild cognitive impairment and alzheimer disease. Ann. Neurol. 2014 Dec;76(6):813-25.
Garzetti L, Menon R, Finardi A, Bergami A, Sica A, Martino G, Comi G, Verderio C, Farina C, Furlan R. Activated macrophages release microvesicles containing polarized M1 or M2 mRNAs. J Leuk Biol. 2014 May;95(5):817-825.
Verderio C, Muzio L, Turola E, Bergami A, Novellino L, Ruffini F, Riganti L, Corradini I, Francolini M, Garzetti L, Maiorino C, Servida F, Vercelli A, Dalla Libera D, Martinelli V, Comi G, Martino G, Matteoli M, Furlan R. Myeloid microvesicles are a marker and therapeutic target for neuroinflammation. Ann. Neurol. 2012 72:610-624.
Dalla Libera D, Di Mitri D, Bergami A, Centonze D, Gasperini C, Grasso MG, Galgani S, Martinelli V, Comi G, Martino G, Borsellino G, Sallusto F, Battistini L, Furlan G. T regulatory cells are markers of disease activity in MS patients. PloS One. 2011 6:e21386.
Esposito M, Ruffini F, Bergami A, Garzetti L, Borsellino G, Battistini L, Martino G, Furlan R. IL-17 and IFN-γ secreting FoxP3 + T cells infiltrate the target tissue in experimental autoimmunity. J Immunol. 2010 185:7467-73.
De Santis G, Ferracin M, Biondani A, Caniatti L, Tola MR, Castellazzi M, Zagatti B, Battistini L, Borsellino G, Fainardi E, Gavioli R, Negrini M, Furlan R*, Granieri E. Altered miRNA expression in T regulatory cells in course of Multiple Sclerosis. J Neuroimmunol. 2010 226:165-71.
Centonze D, Muzio L, Rossi S, Cavasinni F, De Chiara V, Bergami A, Musella A, D’amelio M, Cavallucci V, Martorana A, Bergamaschi A, Cencioni Mt, Butti E, Comi G, Bernardi G, Cecconi F, Battistini L, Furlan R, Martino G. Inflammation triggers synaptic alteration and degeneration in experimental autoimmune encephalomyelitis. J Neurosci. 2009 29:3442-52.
