April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Complete Freunds Adjuvant can protect from Retinal Autoimmunity by an Interleukin-10 dependent mechanism
Author Affiliations & Notes
  • Rafael S Grajewski
    Department of Ophthalmology, University of Cologne, Cologne, Germany
  • Rebecca Scholz
    Department of Ophthalmology, University of Cologne, Cologne, Germany
  • Deniz Hos
    Department of Ophthalmology, University of Cologne, Cologne, Germany
  • Claus Cursiefen
    Department of Ophthalmology, University of Cologne, Cologne, Germany
  • Ludwig M. Heindl
    Department of Ophthalmology, University of Cologne, Cologne, Germany
  • Footnotes
    Commercial Relationships Rafael Grajewski, None; Rebecca Scholz, None; Deniz Hos, None; Claus Cursiefen, None; Ludwig Heindl, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2496. doi:
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      Rafael S Grajewski, Rebecca Scholz, Deniz Hos, Claus Cursiefen, Ludwig M. Heindl; Complete Freunds Adjuvant can protect from Retinal Autoimmunity by an Interleukin-10 dependent mechanism. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2496.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Complete Freunds Adjuvant (CFA) is an oily emulsion with mycobacterial components that is used as an adjuvant to induce antigen-specific autoimmunity, such as experimental autoimmune uveitis (EAU). Our previous work demonstrated that CFA is also capable of non-specific activation of regulatory T cells (Treg). The purpose of the present study was to analyze the immunoregulatory properties of CFA in EAU.

Methods: Wild-type (WT) and IL-10 knockout (KO) C57Bl/6 mice were pre-treated by subcutaneous injection of CFA or Incomplete Freunds Adjuvant (IFA) seven days before induction of EAU by immunization with IRBP peptide 1-20 emulsified in CFA and with Pertussis-Toxin (PTX). EAU scores (scale ranging in severity from 0= no disease to 4 = complete retinal destruction) and associated immunological responses (delayed type hypersensitivity, DTH) were examined.

Results: Pre-treatment with CFA in WT mice (CFA/WT) significantly reduced incidence (p=0.049) and severity (p=0.005) of EAU compared to IFA pre-treatment (IFA/WT). Conversely, pre-treatment of KO mice with CFA (CFA/KO) did not alter incidence and severity of EAU, when compared to IFA pre-treatment of KO mice (IFA/KO). Comparably, the DTH response was significantly lower in the CFA/WT than in the IFA/WT group (p=0.016) and not significantly different in the CFA/KO versus the IFA/KO group. EAU scores and incidence, as well as DTH were not statistically different between the control groups of the two mouse strains (IFA/WT versus IFA/KO).

Conclusions: Although CFA is needed to induce EAU, it partially also has immunosuppressive properties that may be utilized, when it is administered before immunization with antigen. This effect seems to represent an active immunosuppressive mechanism rather than being due to passive exhaustion of effector mechanisms, because it is dependent on the presence of IL-10.

Keywords: 746 uveitis-clinical/animal model • 432 autoimmune disease • 555 immunomodulation/immunoregulation  
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