Gut commensalism, cytokines, and central nervous system demyelination

Kiel Telesford, Javier Ochoa-Repáraz, Lloyd H. Kasper

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

There is increasing support for the importance of risk factors such as genetic makeup, obesity, smoking, vitamin D insufficiency, and antibiotic exposure contributing to the development of autoimmune diseases, including human multiple sclerosis (MS). Perhaps the greatest environmental risk factor associated with the development of immune-mediated conditions is the gut microbiome. Microbial and helminthic agents are active participants in shaping the immune systems of their hosts. This concept is continually reinforced by studies in the burgeoning area of commensal-mediated immunomodulation. The clinical importance of these findings for MS is suggested by both their participation in disease and, perhaps of greater clinical importance, attenuation of disease severity. Observations made in murine models of central nervous system demyelinating disease and a limited number of small studies in human MS suggest that immune homeostasis within the gut microbiome may be of paramount importance in maintaining a disease-free state. This review describes three immunological factors associated with the gut microbiome that are central to cytokine network activities in MS pathogenesis: T helper cell polarization, T regulatory cell function, and B cell activity. Comparisons are drawn between the regulatory mechanisms attributed to first-line therapies and those described in commensal-mediated amelioration of central nervous system demyelination.

Original languageEnglish
Pages (from-to)605-614
Number of pages10
JournalJournal of Interferon and Cytokine Research
Volume34
Issue number8
DOIs
StatePublished - 1 Aug 2014

EGS Disciplines

  • Biology

Fingerprint

Dive into the research topics of 'Gut commensalism, cytokines, and central nervous system demyelination'. Together they form a unique fingerprint.

Cite this