J Immunol. 2012 Nov 1;189(9):4602-11. doi: 10.4049/jimmunol.1200486. Epub 2012 Sep 24. Ren Z, Wang Y, Duan T, Patel J, Liggett T, Loda E, Brahma S,…
Ren Z, Wang Y, Duan T, Patel J, Liggett T, Loda E, Brahma S, Goswami R, Grouse C, Byrne R, Stefoski D, Javed A, Miller…
Aquaporin 4-specific T cells in neuromyelitis optica exhibit a Th17 bias and recognize Clostridium ABC transporter. Varrin-Doyer M, Spencer CM, Schulze-Topphoff U, Nelson PA, Stroud RM, C Cree BA, Zamvil SS.
Fazio R et al. – Neuromyelitis optica (NMO) is a rare demyelinating disease, affecting selectively the optic nerve and the spinal cord. It was previously considered to be a severe variant of multiple sclerosis (MS) due to the similar pathological features and its resemblance to optico–spinal, or Japanese, MS, typical of Asian populations.
BACKGROUND: The role of different chemokine receptors in the pathogenesis of multiple sclerosis (MS) has been extensively investigated; however, little is known about the difference in the role of chemokine receptors between the pathogenesis of neuromyelitis optica (NMO) and MS. Therefore, we examined the expression of chemokine receptors on peripheral blood lymphocytes (PBL) in MS and NMO. METHODS: We used flow cytometry to analyse lymphocyte subsets in 12 patients with relapsing NMO, 24 with relapsing-remitting MS during relapse, 3 with NMO and 5 with MS during remission.
Multiple sclerosis is an inflammatory demyelinating disorder of the CNS. Recent studies have suggested diverse mechanisms as underlying demyelination, including a subset of lesions induced by an interaction between metabolic insult to oligodendrocytes and inflammatory mediators
Matrix metalloproteinase-9 (MMP-9) plays an important role in some neuroinflammatory diseases through the blood-brain barrier (BBB) disruption.
Neuromyelitis optica (NMO) is an inflammatory disease mainly affecting the optic nerve and spinal cord.
In order to clarify the immunological characteristics of multiple sclerosis (MS) and neuromyelitis optica (NMO), we analyzed CD3, CD4, CD8, CD20, CD4(+)CD25(+), CD4(+)CD29(+), and CD8(+)CD11a(high) cells in peripheral blood from patients with MS (16 stable, 6 active) and NMO (15 stable, 7 active), as well as 9 with NMO spectrum, 6 with clinically isolated syndrome (CIS), and 13 with other neurological diseases using flow cytometry. Significant decreases in the numbers of CD8(+) CD11a(high) cells were observed in stable and active MS and CIS
There is a complex, diverse array of “preceding environmental events” and perhaps unconnected immune-related events which are often associated with the period before patients are diagnosed with NMO. In this review we discuss in detail how the different isoform structures of AQP4 in different membrane locales and in different cell types might be related to pathology. Changes in AQP4 expression in CNS and non-CNS tissue can be regulated by inflammatory mediators induced during and following infection or by underlying autoimmunity and can result in the induction of AQP4-specific lymphocytes and ensuing pathogenesis.
There is evidence that the presence of Aquaporin-4 is directly involved in the pathogenesis ofNMO. AQP-4 Ab is thought to bind to an extra-ceLlular domain of the target protein and the E-loop was suggested as a probable candidate epitope. Molecular mimicry namely structural similarity between epitopes contained within microbial and host proteins, leading to cross-reactive Ab’s in the host has been discussed.