Abstract
Mycobacteria in complete Freund's adjuvant (CFA) are an essential component of immunization protocols in a number of autoimmune disease animal models including experimental autoimmune encephalomyelitis and uveoretinitis (EAE and EAU, respectively). We determined the role in EAU of two C-type lectin receptors on myeloid cells that recognize and respond to mycobacteria. Using receptor-specific antibodies and knockout mice, we demonstrated for the first time that the macrophage mannose receptor delays disease development but does not affect severity. In contrast, dectin-1 is critically involved in the development of CFA-mediated EAU. Disease severity is reduced in dectin-1 knockout mice and antibody blockade of dectin-1 during the induction, but not the effector phase, prevents EAU development. Significantly, similar blockade of dectin-1 in vivo has no effect in non-CFA-mediated, spontaneously induced or adoptive transfer models of EAU. Thus dectin-1 plays a critical role in the ability of complete Freund's adjuvant to induce EAU in mice.
Original language | English |
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Pages (from-to) | 398-406 |
Number of pages | 9 |
Journal | Molecular Immunology |
Volume | 67 |
Issue number | 2 B |
Early online date | 26 Jul 2015 |
DOIs | |
Publication status | Published - Oct 2015 |
Keywords
- macrophage mannose receptor
- dectin-1
- mycobacteria
- experimental autoimmune uveitis
- pattern recognition receptor
- adjuvant