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 Experiment Videos

Nervous system-immune system communication.

B G Arnason1

  • 1Department of Neurology, University of Chicago, Illinois 60637.

Reviews of Infectious Diseases
|January 1, 1991
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

The use of mitoxantrone (Novantrone) for the treatment of multiple sclerosis [RETIRED]: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

Neurology·2003
Same author

Design and expression of polymeric immunoglobulin fusion proteins: a strategy for targeting low-affinity Fcgamma receptors.

Protein expression and purification·2001
Same author

Etretinate augments interferon beta-1b effects on suppressor cells in multiple sclerosis.

Archives of neurology·2001
Same author

Interactions between the sympathetic nervous system and the immune system.

Brain, behavior, and immunity·1999
Same author

Treatment of multiple sclerosis with interferon beta.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·1999
Same author

Immunologic therapy of multiple sclerosis.

Annual review of medicine·1999
Same journal

Fatal necrotizing otitis externa in a patient with AIDS.

Reviews of infectious diseases·1991
Same journal

Use of the polymerase chain reaction for the specific and direct detection of Clostridium difficile in human feces.

Reviews of infectious diseases·1991
Same journal

A new case of meningitis due to Pasteurella multocida.

Reviews of infectious diseases·1991
Same journal

Disseminated pelvic actinomycosis presenting as metastatic carcinoma: association with the progestasert intrauterine device.

Reviews of infectious diseases·1991
Same journal

Genetically engineered attenuated herpes simplex viruses.

Reviews of infectious diseases·1991
Same journal

Role of altered drug metabolism in virus-drug interactions.

Reviews of infectious diseases·1991
See all related articles

Certain individuals may have a biological predisposition to develop chronic fatigue syndrome following infection, involving immune system responses. Measuring specific biochemical markers could test this premise in patients and controls.

Area of Science:

  • Neuroimmunology
  • Immunology
  • Endocrinology

Background:

  • Chronic fatigue syndrome (CFS) may stem from a biologically determined susceptibility to infection.
  • The immune system plays a crucial role in the pathological response to infection in susceptible individuals.
  • Interactions between the immune and nervous systems are implicated in the development of CFS.

Purpose of the Study:

  • To review biochemical pathways linking the immune and nervous systems in the context of CFS.
  • To highlight the role of key circulating substances in this immune-nervous system interaction.
  • To propose a method for testing the hypothesis of biological predisposition to CFS.

Main Methods:

  • Review of existing literature on neuroimmunology and CFS.

Related Experiment Videos

  • Identification of biochemical pathways connecting immune and nervous system functions.
  • Discussion of the role of specific biomarkers such as interleukin-1, pituitary hormones, and catecholamines.

    • Main Results:

    • Biochemical pathways exist between the immune and nervous systems.
    • Circulating substances like interleukin-1, pituitary hormones, and catecholamines are key mediators.
    • These pathways may explain the manifestation of disease following infection in susceptible individuals.

    Conclusions:

    • A biologically determined propensity to develop CFS after infection is a plausible hypothesis.
    • Measuring levels of specific biomarkers (interleukin-1, pituitary hormones, catecholamines) in patients and controls can test this hypothesis.
    • Further research into neuroimmune interactions is warranted for understanding and potentially treating CFS.