Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cognition in multiple sclerosis within the modern diagnostic and treatment era.

Brain : a journal of neurology·2025
Same author

AI-driven reclassification of multiple sclerosis progression.

Nature medicine·2025
Same author

Depression Polygenicity and Disease Activity and Disability Worsening in Multiple Sclerosis.

Annals of neurology·2025
Same author

Composite Confirmed Disability Worsening/Progression Is a Useful Clinical Endpoint for Multiple Sclerosis Clinical Trials.

Neurology·2025
Same author

Polygenic liability for anxiety in association with comorbid anxiety in multiple sclerosis.

Annals of clinical and translational neurology·2024
Same author

Worsening MS-A reappraisal of how we characterize the MS disease course.

Multiple sclerosis (Houndmills, Basingstoke, England)·2023

Related Experiment Video

Updated: May 15, 2026

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma
06:15

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma

Published on: October 27, 2014

Interferon beta and glatiramer acetate therapy.

Corey A McGraw1, Fred D Lublin

  • 1Department of Neurology, Albert Einstein College of Medicine, Division of Multiple Sclerosis, Montefiore Medical Center, 111 E 210th St, Bronx, NY 10467, USA. comcgraw@montefiore.org

Neurotherapeutics : the Journal of the American Society for Experimental Neurotherapeutics
|December 25, 2012
PubMed
Summary

Interferon beta and glatiramer acetate are established treatments for relapsing-remitting multiple sclerosis. This review covers their development, mechanisms, clinical trials, and future role among evolving therapies.

More Related Videos

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice

Published on: January 31, 2020

Related Experiment Videos

Last Updated: May 15, 2026

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma
06:15

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma

Published on: October 27, 2014

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice

Published on: January 31, 2020

Area of Science:

  • Neuroimmunology
  • Pharmacology

Background:

  • Interferon beta and glatiramer acetate have been primary treatments for relapsing-remitting multiple sclerosis (RRMS) for 20 years.
  • Understanding these disease-modifying therapies has driven advances in immunology and clinical trial design for MS.

Purpose of the Study:

  • To review the history, mechanisms of action, and clinical use of interferon beta and glatiramer acetate in RRMS.
  • To evaluate the efficacy, tolerability, and side effect profiles of these foundational MS treatments.

Main Methods:

  • Review of historical development and pivotal clinical trials.
  • Analysis of scientific literature on mechanisms of action.
  • Evaluation of clinical data on efficacy and safety.

Main Results:

  • Interferon beta and glatiramer acetate have established roles in managing RRMS, supported by extensive clinical trial data.
  • Their mechanisms of action, while partly understood, continue to be areas of research.
  • These therapies demonstrate varying efficacy and side effect profiles.

Conclusions:

  • Interferon beta and glatiramer acetate remain important options for RRMS treatment.
  • Future research will further elucidate their mechanisms and optimize their use.
  • The evolving landscape of MS therapeutics includes these established drugs alongside newer agents.