Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5916663 | Molecular Immunology | 2015 | 9 Pages |
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.
Keywords
p.ipost immunizationRLRIRBPNLRCLRPRRPAMPEAEMYD88EAUexperimental autoimmune encephalitisAdjuvantpathogen-associated molecular patternSykhen egg lysozymeTransgeniccaspase recruitment domainDectin-1Dendritic cellsspleen tyrosine kinaseMycobacteriawild typemyeloid differentiation primary response gene 88CARDHELC-type lectin receptorMacrophage mannose receptorPRR, Pattern recognition receptorexperimental autoimmune uveitisExperimental autoimmune uveoretinitis
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Authors
Sandra Stoppelkamp, Delyth M. Reid, Joyce Yeoh, Julie Taylor, Emma J. McKenzie, Gordon D. Brown, Siamon Gordon, John V. Forrester, Simon Y.C. Wong,