Antibodies In Multiple Sclerosis Research Articles

A Comprehensive Review of Anti-CD20 Monoclonal Antibodies in Multiple Sclerosis

A Comprehensive Review of Anti-CD20 Monoclonal Antibodies in Multiple Sclerosis

Infectious issues of therapeutic monoclonal antibodies in multiple sclerosis and neuromyelitis optica spectrum disorders

AbstractVarious effective monoclonal antibodies (mAbs) have been approved for both multiple sclerosis (MS) and anti‐aquaporin‐4‐seropositive neuromyelitis optica spectrum disorders worldwide, including in Japan. As these newer mAbs have distinct modes of action that effectively suppress the recurrence of inflammation and slow disability progression, they can modulate and interfere with the protective immune response against pathogens, resulting in various infectious complications. Among various mAbs, natalizumab (NTZ) has the highest risk of causing progressive multifocal leukoencephalopathy (PML), a rare but fatal opportunistic brain infection caused by John Cunningham polyomavirus. Switching from NTZ to B‐cell‐depleting mAbs, such as ocrelizumab, is also a possible risk factor for PML development. Alemtuzumab carries the risk of reactivation of varicella‐zoster virus (VZV); therefore, prophylactic acyclovir treatment is required. NTZ has also been associated with VZV reactivation. Eculizumab can cause severe meningococcal infection due to Neisseria meningitis, and vaccination prior to treatment induction is required. Attention to the reactivation of hepatitis B or Mycobacterium tuberculosis is also needed during mAb therapy. Additionally, in the era of severe acute respiratory syndrome coronavirus 2 infection (COVID‐19), the risk for of developing severe COVID‐19 may be associated with some mAbs, such as B‐cell‐depleting agents. Thorough understanding and mitigation strategies for infectious risks are essential.

Relevance of Pathogenetic Mechanisms to Clinical Effectiveness of B-Cell-Depleting Monoclonal Antibodies in Multiple Sclerosis.

Evidence of the effectiveness of B-cell-depleting monoclonal antibodies (mAbs) in multiple sclerosis (MS) prompted a partial revisitation of the pathogenetic paradigm of the disease, which was, so far, considered a T-cell-mediated autoimmune disorder. Mechanisms underlying the efficacy of B-cell-depleting mAbs in MS are still unknown. However, they likely involve the impairment of pleiotropic B-cell functions different from antibody secretion, such as their role as antigen-presenting cells during both the primary immune response in the periphery and the secondary response within the central nervous system (CNS). A potential impact of B-cell-depleting mAbs on inflammation compartmentalised within the CNS was also suggested, but little is known about the mechanism underlying this latter phenomenon as no definite evidence was provided so far on the ability of mAbs to cross the blood–brain barrier and reliable biomarkers of compartmentalised inflammation are lacking. The present paper briefly summarises the immunopathogenesis of MS with a focus on onset of autoimmunity and compartmentalisation of the immune response; mechanisms mediating B-cell depletion and underlying the effectiveness of B-cell-depleting mAbs are also discussed.

Therapeutic Effect of Anti-CD52 Monoclonal Antibody in Multiple Sclerosis and Its Animal Models Is Mediated via T Regulatory Cells.

The objective of this study is to determine the mechanism of action of anti-CD52 mAb treatment in patients with relapsing-remitting multiple sclerosis (RRMS). Experimental autoimmune encephalomyelitis (EAE), an animal model of the disease, was used to address the role of T regulatory cells (Tregs) in the anti-CD52 mAb-induced suppression of the disease. In vitro studies on PBMCs from RRMS patients and matched healthy controls determined the effect of IL-7 on the expansion of CD4+CD25+CD127- Tregs and induction of their suppressive phenotype. This study using EAE animal models of MS has shown that mouse anti-CD52 mAb suppression of clinical disease was augmented by coadministration of IL-7 and partially reversed by anti-IL-7 mAb. In vitro human studies showed that IL-7 induced expansion of CD4+CD25+CD127- Tregs and increased their FOXP3, GITIR, CD46, CTLA-4, granzyme B, and perforin expression. Anti-CD52 mAb treatment of mice with relapsing-remitting EAE induced expansion of Foxp3+CD4+ Tregs and the suppression of IL-17A+CD4+ and IFN-γ+CD4+ cells in peripheral immune organs and CNS infiltrates. The effect was detected immediately after the treatment and maintained over long-term follow-up. Foxp3+CD4+ Treg-mediated suppression of IL-17A+CD4+ and IFN-γ+CD4+ cells in the spinal cord infiltrates was reversed after inducible Foxp3 depletion. Our results demonstrated that the therapeutic effect of U.S. Food and Drug Administration-approved anti-CD52 mAb is dependent on the presence of Tregs.

Prevalence of SARS-CoV-2 antibodies in multiple sclerosis: The hidden part of the iceberg

Background. We compared the prevalence of SARS-CoV-2 IgG/IgM in multiple sclerosis (MS), low-risk, and high-risk populations and explored possible clinical correlates. Methods. In this cross-sectional study, we recruited MS patients, low-risk (university staff from non-clinical departments), and high-risk individuals (healthcare staff from COVID-19 wards) from 11 May to 15 June 2020. We used lateral flow immunoassay to detect SARS-CoV-2 IgG and IgM. We used t-test, Fisher’s exact test, chi square test, or McNemar’s test, as appropriate, to evaluate between-group differences. Results. We recruited 310 MS patients (42.3 ± 12.4 years; females 67.1%), 862 low-risk individuals (42.9 ± 13.3 years; females 47.8%), and 235 high-risk individuals (39.4 ± 10.9 years; females 54.5%). The prevalence of SARS-CoV-2 IgG/IgM in MS patients (n = 9, 2.9%) was significantly lower than in the high-risk population (n = 25, 10.6%) (p < 0.001), and similar to the low-risk population (n = 11, 1.3%) (p = 0.057); these results were also confirmed after random matching by age and sex (1:1:1). No significant differences were found in demographic, clinical, treatment, and laboratory features. Among MS patients positive to SARS-CoV-2 IgG/IgM (n = 9), only two patients retrospectively reported mild and short-lasting COVID-19 symptoms. Conclusions. MS patients have similar risk of SARS-CoV-2 infection to the general population, and can be asymptomatic from COVID-19, also if using treatments with systemic immunosuppression.

Antigen-specific tolerization in human autoimmunity: Inhibition of interferon-beta1a anti-drug antibodies in multiple sclerosis: A case report

Background: Antigen-specific tolerance in auto-immune diseases is the goal for effective treatment with minimal side-effects. Whilst this is achievable in animal models, notably via intravenous delivery of the model-specific autoantigen following transient CD4 T cell depletion, specific multiple sclerosis autoantigens remain unproven. However, anti-drug antibodies to human therapeutic proteins represent a model human autoimmune condition, which may be used to examine immune-tolerance induction. Some people with MS (PwMS) on interferon-beta1a (IFNβ1a) develop neutralizing antibodies to IFNβ1a that do not disappear in repeated tests over years.Methods: One PwMS was recruited, as part of a planned phase IIa trial (n = 15), who had developed neutralizing antibodies to subcutaneous IFNβ1a. Mitoxantrone (12 mg/m2) was administered as a lymphocyte depleting agent followed by four days of (88 μg/day + three 132 μg/day) intravenous IFNβ1a. Subcutaneous IFNβ1a three times a week was maintained during follow-up. IFNβ1a neutralizing antibody responses in serum were measured during treatment and three-monthly for 12 months.Findings: One participant was recruited and, within 6 months of tolerization, the neutralizing antibodies were undetectable. The tolerization treatment was well tolerated. However, the study was terminated after the first enrolment, on ethical grounds, as treatment alternatives became available and the potential risks of mitoxantrone use increased.Interpretation: The data suggest that it may be possible to induce antigen-specific tolerance by providing tolerogenic antigen following transient immune depletion. Further studies are warranted.Funding: The study was supported by an unrestricted research grant from Merck-Serono.

Gluten intolerance antibodies in multiple sclerosis and clinically isolated syndrome : Coexistent or coincidental?

AbstractObjectiveAs it is well known that autoimmune diseases can coexist, the association of multiple sclerosis (MS) with other autoimmune diseases has always been a major concern for clinicians. In this study, we aimed to investigate the clinical findings, and the frequency of autoantibodies related to celiac disease in MS and clinically isolated syndrome (CIS).MethodsAnti‐gliadin immunoglobulin A and anti‐gliadin immunoglobulin G and anti‐endomysium immunoglobulin A and anti‐endomysium immunoglobulin G antibodies were studied by the indirect immune fluorescence method, anti‐tissue transglutaminase immunoglobulin A and anti‐tissue transglutaminase immunoglobulin G were studied by enzyme‐linked immunosorbent assay. The study included 30 patients with CIS, 50 patients with relapsing–remitting MS (RRMS), 30 patients with progressive MS (PMS) and 42 healthy individuals as the control group.ResultsOne patient was anti‐gliadin immunoglobulin A‐positive in the CIS group, four patients in the RRMS group, one patient in the PMS group and two patients in the control group. Four patients were anti‐gliadin immunoglobulin G‐positive in the CIS group, four patients in the RRMS group, three patients in the PMS group and three patients in the control group. One patient was anti‐endomysium immunoglobulin A‐positive in the CIS group and two patients in the RRMS group. Two patients were anti‐endomysium immunoglobulin G‐positive in the CIS group, one patient in the RRMS group and one patient in the PMS group. Three patients were anti‐tissue transglutaminase immunoglobulin A‐positive in the RRMS group and two patients in the control group. All groups were anti‐tissue transglutaminase immunoglobulin G‐negative. Although the number of patients with positive antibodies seemed to be higher in MS groups, the difference was not statistically significant between the groups.ConclusionWe observed that celiac antibodies were not more common in MS patients than healthy controls. However, these antibodies are important to suggest gastrointestinal complaints in MS patients.

Ocrelizumab depletes T-lymphocytes more than rituximab in multiple sclerosis

We aim to directly compare changes in lymphocyte subpopulations between chimeric (rituximab) and humanised (ocrelizumab) anti-CD20 antibodies in multiple sclerosis (MS). In this retrospective analysis of prospectively collected data, we included 88 patients with MS, treated with rituximab (n=50) or ocrelizumab (n=38). We used flow cytometry in the peripheral blood to count total lymphocytes and lymphocytes expressing different phenotypic markers (CD4, CD8, CD19, CD20, CD4/CD8 ratio), before treatment and after 1, 3 and 6 months. On linear mixed effect regression models, after 1, 3 and 6 months, patients treated with rituximab and with ocrelizumab were similar in total lymphocyte count, CD19 lymphocytes, CD20 lymphocytes and CD4/CD8 ratio. However, patients treated with ocrelizumab presented with lower CD4 T lymphocytes and CD8 T lymphocytes after 1, 3 and 6 months (all p<0.05). No between-treatment difference in EDSS progression was found. B-cell levels in the peripheral blood were equally decreased by rituximab and ocrelizumab. On the contrary, CD4 and CD8 T lymphocyte reduction was more pronounced in ocrelizumab, when compared with rituximab, suggesting a broader immunomodulatory effect for the humanised antibody to be confirmed and correlated with clinical efficacy in the long term.

Anti-Kir4.1 Antibodies in Multiple Sclerosis: Specificity and Pathogenicity.

The glial cells in the central nervous system express diverse inward rectifying potassium channels (Kir). They express multiple Kir channel subtypes that are likely to have distinct functional roles related to their differences in conductance, and sensitivity to intracellular and extracellular factors. Dysfunction in a major astrocyte potassium channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurological diseases. The autoimmune effects on the potassium channel have not yet been fully described in the literature. However, several research groups have reported that the potassium channels are an immune target in patients with various neurological disorders. In 2012, Srivastava et al. reported about Kir4.1, a new immune target for autoantibodies in patients with multiple sclerosis (MS). Follow-up studies have been conducted by several research groups, but no clear conclusion has been reached. Most follow-up studies, including ours, have reported that the prevalence of Kir4.1-seropositive patients with MS was lower than that in the initial study. Therefore, we extensively review studies on the method of antibody testing, seroprevalence of MS, and other neurological diseases in patients with MS. Finally, based on the role of Kir4.1 in MS, we consider whether it could be an immune target in this disease.

Prevalence of SARS-CoV-2 Antibodies in Multiple Sclerosis: The Hidden Part of the Iceberg.

Background. We compared the prevalence of SARS-CoV-2 IgG/IgM in multiple sclerosis (MS), low-risk, and high-risk populations and explored possible clinical correlates. Methods. In this cross-sectional study, we recruited MS patients, low-risk (university staff from non-clinical departments), and high-risk individuals (healthcare staff from COVID-19 wards) from 11 May to 15 June 2020. We used lateral flow immunoassay to detect SARS-CoV-2 IgG and IgM. We used t-test, Fisher’s exact test, chi square test, or McNemar’s test, as appropriate, to evaluate between-group differences. Results. We recruited 310 MS patients (42.3 ± 12.4 years; females 67.1%), 862 low-risk individuals (42.9 ± 13.3 years; females 47.8%), and 235 high-risk individuals (39.4 ± 10.9 years; females 54.5%). The prevalence of SARS-CoV-2 IgG/IgM in MS patients (n = 9, 2.9%) was significantly lower than in the high-risk population (n = 25, 10.6%) (p < 0.001), and similar to the low-risk population (n = 11, 1.3%) (p = 0.057); these results were also confirmed after random matching by age and sex (1:1:1). No significant differences were found in demographic, clinical, treatment, and laboratory features. Among MS patients positive to SARS-CoV-2 IgG/IgM (n = 9), only two patients retrospectively reported mild and short-lasting COVID-19 symptoms. Conclusions. MS patients have similar risk of SARS-CoV-2 infection to the general population, and can be asymptomatic from COVID-19, also if using treatments with systemic immunosuppression.

Increased frequency of canine distemper virus-specific antibodies in multiple sclerosis.

Background and purposeCanine distemper virus (CDV) is a candidate agent in the etiology of multiple sclerosis (MS). Elevated anti‐CDV levels were previously found in the sera from MS patients compared with controls. We now investigated whether there was an age‐related association with the presence of antibodies specific to CDV‐hemagglutinin (H) protein in MS.MethodsSera from patients with MS, other neurological diseases, and inflammatory and/or autoimmune diseases, and healthy individuals were screened for anti‐CDV in an ELISA using linear peptides of the CDV‐H protein as antigen. Antibody levels to measles and varicella‐zoster virus were measured and served as controls.ResultsAnalysis of the new cohort of MS patients and controls confirmed our initial finding of elevated anti‐CDV‐H levels in MS patients. An increase in measles but not varicella‐zoster virus antibody levels was found in MS patients compared with healthy controls. Data from the new cohort of patients and controls were combined with data from the original study and analyzed with respect to age distribution of anti‐CDV IgG. Mean CDV antibody levels were significantly elevated in each decade from 20 to 50 years of age in MS compared with healthy and disease controls. Antibody levels to measles virus were not consistently elevated during this age span. A striking relationship (p < .0001, odds ratio = 5.0) was observed between elevated anti‐CDV‐H levels and diagnosis of MS.ConclusionsThe finding that anti‐CDV levels are elevated in MS patients of all ages provides substantial evidence of a strong association between elevated anti‐CDV and MS.

A Multiple N-Glucosylated Peptide Epitope Efficiently Detecting Antibodies in Multiple Sclerosis.

Diagnostics of Multiple Sclerosis (MS) are essentially based on the gold standard magnetic resonance imaging. Few alternative simple assays are available to follow up disease activity. Considering that the disease can remain elusive for years, identification of antibodies fluctuating in biological fluids as relevant biomarkers of immune response is a challenge. In previous studies, we reported that anti-N-glucosylated (N-Glc) peptide antibodies that can be easily detected in Solid-Phase Enzyme-Linked ImmunoSorbent Assays (SP-ELISA) on MS patients’ sera preferentially recognize hyperglucosylated adhesin of non-typeable Haemophilus Influenzae. Since multivalency can be useful for diagnostic purposes to allow an efficient coating in ELISA, we report herein the development of a collection of Multiple N-glucosylated Peptide Epitopes (N-Glc MEPs) to detect anti-N-Glc antibodies in MS. To this aim, a series of N-Glc peptide antigens to be represented in the N-GlcMEPs were tested in competitive ELISA. We confirmed that the epitope recognized by antibodies shall contain at least 5-mer sequences including the fundamental N-Glc moiety. Using a 4-branched dendrimeric lysine scaffold, we selected the N-Glc MEP 24, carrying the minimal epitope Asn(Glc) anchored to a polyethylene glycol-based spacer (PEG) containing a 19-atoms chain, as an efficient multivalent probe to reveal specific and high affinity anti-N-Glc antibodies in MS.

Frequency of myelin oligodendrocyte glycoprotein antibody in multiple sclerosis: A multicenter cross-sectional study.

ObjectiveTo address the frequency of myelin oligodendrocyte glycoprotein (MOG) antibody (Ab) in an unselected large cohort of adults with MS.MethodsThis is a cross-sectional study in 2 MS expert centers (Lyon and Strasbourg University Hospitals, France) between December 1, 2017, and June 31, 2018. Patients aged ≥18 years with a definite diagnosis of MS according to 2010 McDonald criteria were tested for MOG-Ab by using a cell-based assay (CBA) in Lyon and subsequently included. Positive samples were tested by investigators blinded to the first result with a second assay in a different laboratory (Barcelona, Spain) by using the same plasmid and secondary Ab.ResultsSerum samples from 685 consecutive patients with MS were analyzed for MOG-Ab. Median disease duration at sampling was 11.5 (interquartile range, 5.8–17.7) years, and 72% were women. Two (0.3%) patients resulted to be MOG-Ab-positive. The 2 patients were women aged 42 and 38 at disease onset and were diagnosed with secondary and primary progressive forms of MS, respectively. This positive result was confirmed by the CBA in Barcelona.ConclusionOur findings indicate that MOG-Ab are exceptional in MS phenotype, suggesting that the MOG-Ab testing should not be performed in typical MS presentation.

Mechanisms of activation induced by antiphospholipid antibodies in multiple sclerosis: Potential biomarkers of disease?

Multiple sclerosis (MS) is a chronic, multifactorial, inflammatory disease of the central nervous system where demyelination leads to neurodegeneration and disability. The pathogenesis of MS is incompletely understood, with prevalence of antiphospholipid antibodies (aPL) speculated to contribute to MS pathogenesis. In fact, MS shares common clinical features with the Antiphospholipid Syndrome (APS) such as venous thromboembolism. Consequently, the presence of aPL which are associated with blood clot formation in the APS need to be further investigated for a possible pro-coagulant role in the development of thrombosis in MS. The effects of IgG aPL from patients with MS upon astrocyte activation has never been characterized. We purified IgG from 30 subjects. A human astrocytic cell line was treated with 100 μg/ml IgG for 1 h, and cell extracts were examined by immunoblot using antibodies to p38 MAPK and NFκB to further examine intracellular signaling pathways induced by these IgGs. Only IgG from patients who are positive for aPL caused phosphorylation of p38 MAPK and NFκB in astrocytes. These effects were not seen with IgG from patients with MS but with no aPL or healthy controls. Understanding the intracellular mechanism of aPL-mediated astrocyte activation may help to establish new therapeutic approaches, such as selective inhibition of the mitogen-activated protein kinases, to control MS activity or possible thrombotic states.

Monoclonal Antibodies in Multiple Sclerosis: Present and Future.

The global incidence of multiple sclerosis (MS) appears to be increasing. Although it may not be associated with a high mortality rate, this disease has a high morbidity rate which affects the quality of life of patients and reduces their ability to do their activities of daily living. Thankfully, the development of novel disease modifying therapies continues to increase. Monoclonal antibodies (MABs) have become a mainstay of MS treatment and they are likely to continue to be developed for the treatment of this disease. Specifically, MABs have proven to be some of the most efficacious treatments at reducing relapses and the inflammation in MS patients, including the first treatment for primary progressive MS and are being explored as reparative/remyelinating agents as well. These relatively new treatments will be reviewed here to help evaluate their efficacy, adverse events, immunogenicity, and benefit-risk ratios in the treatment of the diverse spectrum of MS. The focus will be on MABs that are currently approved or may be approved in the near future.

Therapeutic Applications of Monoclonal Antibodies in Multiple Sclerosis

Despite the various therapies available, the use of monoclonal antibodies is a highly specific approach that has only recently been of interest to researchers. The properties of antibodies have led to their use in the treatment of various diseases, including cancer, Alzheimer's disease, diabetes and multiple sclerosis (MS). MS, a chronic inflammatory disease, occurs commonly in young adults. The disease is one of the attractive options for monoclonal antibody therapy because it has no definitive drug for its treatment. Antibodies, by targeting different molecules, have different mechanisms to improve the disease. Treatment with monoclonal antibody has culminated in a clear divergence in paradigm and concentration in MS therapeutics. Application of monoclonal antibody in early inflammatory phases can inhibit or postpone the disability in MS subjects. Ocrelizumab and daclizumab are currently under investigation by late phase III trials, and some other monoclonal antibodies are in the early stages of clinical trials. Monoclonal antibodies are of special structural features (including chimeric, humanized, or fully humanized) as well as specific targets (such as stimulation of signal transduction by binding to receptors, blocking interactions, antibody-dependent cell cytotoxicity, complement-dependent cytotoxicity), thus providing various mechanisms of actions during MS therapy. In the present paper, we reviewed different monoclonal antibodies used in MS, their mechanism of action and theirs target molecules.

The Role of B Cells and Antibodies in Multiple Sclerosis, Neuromyelitis Optica, and Related Disorders.

Our pathophysiological concept of the most common central nervous system demyelinating disease, multiple sclerosis, strikingly evolved by recent discoveries suggesting that B lymphocytes substantially contribute in its initiation and chronic propagation. In this regard, activated B cells are nowadays considered to act as important antigen-presenting cells for the activation of T cells and as essential source of pro-inflammatory cytokines. Hereby, they create a milieu in which other immune cells differentiate and join an orchestrated inflammatory infiltration of the CNS. Without a doubt, this scientific leap was critically pioneered by the empirical use of anti-CD20 antibodies in recent clinical MS trials, which revealed that the therapeutic removal of immature and mature B cells basically halted development of new inflammatory flares in otherwise relapsing MS patients. This stabilization occurred largely independent of any indirect effect on plasma cell-produced antibody levels. On the contrary, peripherally produced autoantibodies are probably the most important B cell component in two other CNS demyelinating diseases which are currently in the process of being delineated as separate disease entities. The first one is neuromyelitis optica in which an antibody response against aquaporin-4 targets and destroys astrocytes, the second, likely distinct entity embraces a group of patients containing antibodies against myelin oligodendrocyte glycoprotein. In this review, we will describe and summarize pro-inflammatory B cell properties in these three CNS demyelinating disorders; we will however also provide an overview on the emerging concept that B cells or B cell subsets may exert immunologically counterbalancing properties, which may be therapeutically desirable to maintain and foster in inflammatory CNS demyelination. In an outlook, we will discuss accordingly, how this potentially important aspect can be harnessed to advance future B cell-directed therapeutic approaches in multiple sclerosis and related diseases.

Monoclonal Antibodies for Multiple Sclerosis: An Update.

The use of monoclonal antibodies in multiple sclerosis (MS) patients is in a transitional period. Studies regarding well-established, effective antibodies such as natalizumab and alemtuzumab focus more and more on long-term efficacy and safety, risk management, and treating complications. Primary progressive MS, a disease that was long considered to be unmodifiable, is currently in focus following ocrelizumab being approved as the first drug with a proven beneficial effect on the disease course. Conversely, post-marketing safety mechanisms have also proven to function as daclizumab has been suspended after a series of relevant serious adverse events. Currently, new therapies are emerging that promise more convenience and an improved safety profile (ofatumumab) or remyelinating potential with clinical improvement (opicinumab). While it is very unlikely that monoclonal antibodies will ever cure MS, they have become very valuable therapeutic tools to better patient outcomes. This review focuses on developments of monoclonal antibodies used in the past, present, and near future in MS patients.

Diagnostic value of antibodies to myelin oligodendrocyte glycoprotein in demyelinating diseases of the central nervous system

To evaluate the diagnostic value of MOG-IgG antibodies in multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). Twenty-nine patients with definitive MS according to the criteria of McDonald, 2010 (21 with relapse-remitting MS and 8 with secondary progressive MS), 7 patients with ADEM confirmed by clinical and instrumental data and 27 healthy volunteers were included in the study. Serum MOG-IgG levels were evaluated in all patients. MOG-IgG levels in the cerebrospinal fluid (CSF) were evaluated in 22 cases with MS, 6 cases with ADEM, and 8 healthy volunteers using ELISA. Serum MOG-IgG levels are significantly higher in patients with MS and ADEM compared to the control group. No statistically significant differences in the serum MOG-IgG levels were found between MS and ADEM groups. When analyzing the level of MOG-IgG in CSF, no statistically significant between-group differences were obtained. The sensitivity and specificity of the determination of MOG-IgG in serum in patients with MS are 75,8% and 92.59%, respectively. MOG-IgG is detected in serum and CSF in patients with demyelinating diseases that indicates its pathogenetic significance in the development of MS and ADEM. Serum MOG-IgG may be a valuable biomarker for demyelinating diseases. Further research in a large population of patients is required.

Multiple Sclerosis and Autoreactive Antibodies

Background: The prevalence of auto antibodies in multiple sclerosis (MS) patients and their implications differ between various studies. Our aims were to determine the frequency and type of auto reactive antibodies (ARABS) in a hospital cohort of patients followed for MS and to study the clinical, radiological and progressive features associated with this group.