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Although T cell responses to the quantitatively major myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP), are likely to be of importance in the course of multiple sclerosis (MS), cell-mediated autoimmune responses to other myelin antigens, in particular quantitatively minor myelin antigens, such as myelin-associated glycoprotein (MAG) and the central nervous system-specific myelin oligodendrocyte glycoprotein (MOG), could also play a prevalent role in disease initiation or progression. Highly purified myelin antigens were used in this study to assess cell-mediated immune response to MOG in MS patients, in the context of the reactivity to other myelin antigens, MBP, PLP, and MAG. The greatest incidence of proliferative response by MS peripheral blood lymphocytes was to MOG, as 12 of 24 patients tested reacted and, of these

Multiple sclerosis (MS) is the most common neurological immune-mediated disease leading to disability in young adults. The outcome of the disease is unpredictable, and over time, neurological disabilities accumulate. Interferon beta-1b was the first drug to be approved in the 1990s for relapsing-remitting MS to modulate the course of the disease. Over the past two decades, the treatment landscape has changed tremendously. Currently, more than a dozen drugs representing 1 substances with different mechanisms of action have been approved (interferon beta preparations, glatiramer acetate, fingolimod, siponimod, mitoxantrone, teriflunomide, dimethyl fumarate, cladribine, alemtuzumab, ocrelizumab, and natalizumab). Ocrelizumab was the first medication to be approved for primary progressive MS. The objective of this review is to present the modes of action of these drugs and their effects on the immunopathogenesis of MS. Each agent's clinical development and potential side effects are discussed.

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Objective-To report on four patients with autoimmune disorders who developed acute myocardial infarction (MI) during or soon after treatment with high dose intravenous immunoglobulins (IVIG) and to determine the clinical profile of patients prone to this complication. Methods-The clinical history of the four patients is reported with details concerning age, sex, indication for IVIG treatment, risk factors, timing of the MI and outcome. The relevant medical literature has been reviewed. Results-The patients, three men and one woman, aged 42-67, received IVIG treatment for diVerent autoimmune disorders. All had a history of atherosclerosis or previous risk factors such as hypertension, stroke, hyperlipidaemia and obesity. Two of the patients suVered a MI after the first infusion of IVIG while the others-after the 5th and 15th pulses. MI occurred during the infusion in two patients and after a few days in the others. All the patients recovered from the acute event. These observations are in concert with sporadic cases of IVIG related thrombosis reported in the medical literature. Conclusion-In patients with vascular risk factors such as old age, hypertension, history of stroke or coronary artery disease, the possibility of IVIG related vascular complications should be considered and IVIG prescribed with a cautious reweighted risk/benefit consideration. (Ann Rheum Dis 2000;59:77-80) High dose intravenous immunoglobulin (IVIG) treatment is being increasingly used in a wide range of autoimmune disorders such as Kawasaki, 1 neuroimmunological disorders, [2][3][4] dermatomyositis, 5 vasculitis 6 immune cytopenia and other conditions. 7 8 IVIG have been considered a safe medication, with minor adverse events such as headache, nausea and myalgias, occurring in less than 10% of patients.9 10 With the wider use of IVIG, the reported rate of side eVects has increased, 11 some of them being potentially fatal. 12We describe four patients with autoimmune disorders who developed acute myocardial infarction (MI) a few days after receiving IVIG. Case reports CASE 1The patient is a 60 year old man with relapsing polychondritis of three years duration manifesting as extreme fatigue, recurrent episodes of chondritis of the ears, hoarseness, livedo reticularis, migratory arthritis and myalgias, episcleritis and vestibular neuropathy with vertigo and sensorineural deafness. He had documented arterial hypertension for the past two years. Laboratory tests disclosed an increased erythrocyte sedimentation rate (ESR) (120 mm 1st h) and normocytic normochromic anaemia (Hb 10 g/dl). Immunological tests including anticardiolipin antibodies were negative. The patient was initially treated (at another centre) with prednisone (1 mg/kg) and monthly intravenous cyclophosphamide (800 mg/m 2 ), but repeated attempts to lower the prednisone dose below 25 mg/d resulted in acute exacerbations. Parenteral methotrexate 30 mg/week was prescribed. During this treatment he developed right hemiparesis with evidence of cerebral lacunar infarction on...