Specific Proliferation Towards Myelin Antigens in Patients with Multiple Sclerosis During a Relapse

Abstract

Whether autoreactive T cells from multiple sclerosis (MS) patients display a certain autoreactive pattern is controversial. In this study, we have analyzed reactivity towards myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), alpha B-crystallin and S100beta antigens in 35 relapsing-remitting MS patients and 12 healthy controls (HC). During relapse, we observed T-specific proliferation towards MBP (15.8%), MOG (38.9%), alpha B-crystallin (11.1%) and S100beta (26.3%) in MS patients. Reactivity to MBP (12%), MOG (28%), alpha B-crystallin (28%) and S100beta (19.2%) was also observed in HC. There were changes in the specific proliferation in consecutive samples obtained from either patients or HC. Such fluctuations did not follow any specific or conservative patterns. Antigen-specific cytokine production was also assessed as a method to evaluate whether there were differences in the qualitative response between MS patients and HC, with negative results. In summary, we show here that the reactivity patterns, as measured by specific proliferation and cytokine production, are similar in RR-MS patients and HC and fluctuate over time.

Specific T-cell proliferation to myelin peptides in relapsing-remitting multiple sclerosis

“…T‐cell responses to myelin antigens have been extensively studied in patients with multiple sclerosis (MS) and control subjects [1–6]. Evidence of a direct pathogenic role of auto‐reactive T cells in MS emerged from the conclusions of a clinical trial [7] in which some patients treated with an altered peptide ligand based on the myelin basic protein (MBP) 83–99 epitope developed exacerbations of the disease with a greater degree of brain inflammation and increased anti‐MBP T‐cell responses.…”

Increased prevalence of varicella zoster virus DNA in cerebrospinal fluid from patients with multiple sclerosis

“…Despite numerous efforts and studies carried out over the past several years, the etiology of MS remains unknown, while the clinical and pathogenic features of MS suggest the involvement of unidentified infectious agents in the etiology of the disease [Ferrante and Mancuso, 1996;Dalgleish, 1997;Monteyne et al, 1998;Granieri et al, 2001]. Among such agents, viruses are the most likely candidates because in addition to having a direct role in damage to the CNS during infection, they can induce demyelination through an autoimmune process triggered by molecular mimicry, expression and overexpression of MHC antigens on target cells, and by acting as superantigens [Prat and Martin, 2002;Saez-Torres et al, 2002].…”

Fibroblasts as an Alternative to Mesenchymal Stem Cells with Successful Treatment and Immune Modulation in EAE Model of Multiple Sclerosis

“…It is known that remission is associated with reduction of pathogenic T cells and upregulation of number and activity of T regulatory (Treg) cells (1), while progression is associate with augmentation of myelin-reactive T cells and suppression of Treg activity and number (2). Current treatments for MS include non-specific immune modulators such as Avonex, Capaxone, Rebif, Tysabri and Campath (3). These approaches possess various degrees of toxicity, adverse reactions associated with non-specific immune suppression, as well, display limited efficacy against primary progressive disease.…”