Killam Seminar Series: Compartmentalized Inflammation in Multiple Sclerosis: Hideout of Chronic Immune Response
Supported by the generosity of the Killam Trusts, the MNI's Killam Seminar Series invites outstanding guest speakers whose research is of interest to the scientific community at the MNI and Ï㽶ÊÓƵ.
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Roberta Magliozzi, PhD
Assistant Professor, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Italy
Host:ÌýJo Anne Stratton
´¡²ú²õ³Ù°ù²¹³¦³Ù:ÌýA significant neurodegenerative component characterizes multiple sclerosis, and involves not only plaques but the non-plaque parenchyma as well. It is also becoming increasingly clear that MS inflammation is not only restricted to the initial relapse remitting phases but persist for all the disease duration, hidden within intracerebral niches where it may probably become resistant to current therapies. Therefore compartmentalized inflammation, persisting in intrathecal niches, such as choroid plexus (CP), leptomeninges and perivascular spaces, together with degree of lesion activity, contribute to multiple sclerosis (MS) immunopathology, demyelination and accumulation of disability. However, the exact contribution of these inflammatory components in progressive MS needs further investigation.
The presence and inducible formation of immune-competent niches in the meninges ( ectopic tertiary lymphoid-like structures, TLS), suggests that these aberrant aggregates may support and chronically sustain disease-relevant immune responses in the CNS. TLS-associated immune responses within the leptomeninges are proposed to contribute to ongoing neuropathology of the cortical GM and to disease exacerbation, possibly regulating the balance of pro-inflammatory and anti-inflammatory responses in the meninges. The observation that the immune cell aggregates in the MS meninges appear to be at various stages of development is entirely in keeping with observations from a large number of non-CNS chronic inflammatory conditions, suggesting therefore a key role of meningeal inflammation and TLS in chronic progression.
