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Oral tolerance in EAE: reversal of tolerance by T helper cell cytokines

K A Kelly1, C C Whitacre

  • 1Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock 72205, USA. kkelly@biomed.uams.edu

Insights

Oral administration of myelin basic protein (MBP) impacts immune responses in experimental autoimmune encephalomyelitis (EAE). Cytokines like IL-4 and IL-5 can restore reduced IgA antibody production in Peyer's patches.

Area of Science:

  • Immunology
  • Neuroscience
  • Oral Tolerance

Background:

  • Oral administration of myelin basic protein (MBP) partially reduces experimental autoimmune encephalomyelitis (EAE) symptoms and serum antibody titers.
  • The effect of oral MBP on the distribution and isotype of antibody-forming cells (AFC) in lymphoid tissues is not fully understood.

Purpose of the Study:

  • To investigate how orally administered MBP influences the isotypic distribution of anti-MBP AFC in various lymphoid tissues.
  • To determine the role of cytokines, specifically IL-4 and IL-5, in reconstituting anti-MBP IgA AFC frequencies.

Main Methods:

  • Mice were orally administered MBP.
  • Anti-MBP antibody-forming cells (AFC) were analyzed for isotype distribution in different lymphoid tissues, including Peyer's patches.
  • In vitro cultures were used to assess the effect of IL-4 and IL-5 on anti-MBP IgA AFC frequencies.

Main Results:

  • Oral MBP administration altered the isotypic distribution of anti-MBP AFC, particularly in mucosal tissues.
  • A significant reduction in anti-MBP IgA AFC frequencies was observed in Peyer's patches, while IgM AFC frequencies remained unaffected.
  • Addition of IL-4 and IL-5 reconstituted the anti-MBP IgA AFC frequencies in Peyer's patches without inducing de novo responses.

Conclusions:

  • Oral antigen administration can lead to isotype-selective decreases in antibody production.
  • The observed decrease in anti-MBP IgA AFC frequencies can be reversed by appropriate cytokine exposure (IL-4 and IL-5).
  • This suggests a mechanism for modulating mucosal immune responses through cytokine intervention.

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