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Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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Author Spotlight: Novel Assay for Studying B-Cell Responses in Multiple Sclerosis Research
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Multiple sclerosis reactivation postfingolimod cessation: is it IRIS?

R Alroughani1, A Almulla2, S Lamdhade2

  • 1Division of Neurology, Department of Medicine, Amiri Hospital, Kuwait City, Kuwait Neurology Clinic, Dasman Diabetes Institute, Kuwait City, Kuwait.

BMJ Case Reports
|October 17, 2014
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Summary
This summary is machine-generated.

Fingolimod withdrawal in multiple sclerosis (MS) patients may trigger immune reconstitution inflammatory syndrome (IRIS), causing severe disease reactivation. This highlights the risk of IRIS during washout periods after discontinuing fingolimod therapy.

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Area of Science:

  • Neurology
  • Immunology
  • Pharmacology

Background:

  • Limited data exists on efficacy and safety when switching immunotherapies in multiple sclerosis (MS).
  • The mechanism of rebound activity after fingolimod withdrawal in MS patients remains poorly understood.

Observation:

  • A 36-year-old woman experienced severe MS reactivation 7 weeks after discontinuing fingolimod.
  • Disease reactivation occurred despite no breakthrough during an 8-week natalizumab washout period prior to fingolimod withdrawal.

Findings:

  • Severe reactivation post-fingolimod withdrawal may be attributed to immune reconstitution inflammatory syndrome (IRIS).
  • An abrupt increase in lymphocyte count correlated with the observed IRIS.
  • The clinical and radiological presentation posed diagnostic challenges, including the risk of progressive multifocal leukoencephalopathy.

Implications:

  • Patients discontinuing fingolimod may be at risk for IRIS and subsequent disease reactivation.
  • Understanding IRIS is crucial for managing patients with multiple sclerosis during immunotherapy transitions.
  • This case underscores the need for vigilance regarding potential immune reconstitution inflammatory syndrome following fingolimod cessation.