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Mannosylated self-peptide inhibits the development of experimental autoimmune encephalomyelitis via expansion of nonencephalitogenic T cells

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Author: Kel, J.M. · Slütter, B. · Drijfhout, J.W. · Koning, F. · Nagelkerken, L.
Type:article
Date:2008
Institution: TNO Kwaliteit van Leven
Source:Journal of Leukocyte Biology, 1, 84, 182-190
Identifier: 240889
doi: doi:10.1189/jlb.0507312
Keywords: Biology · Biomedical Research · C-type lectins · Delayed-type hypersensitivity (DTH) · Tolerance · chemokine · cytokine · pertussis toxin · protein m plp139 151 · protein plp139 151 · proteolipid protein · adoptive transfer · allergic encephalomyelitis · animal cell · animal experiment · antigen specificity · article · autoimmunity · CD4+ T lymphocyte · clonogenesis · controlled study · cytokine production · delayed hypersensitivity · drug inhibition · drug tolerance · effector cell · female · immunization · immunocompetent cell · lymphocyte transformation · mouse · nonhuman · priority journal · T lymphocyte · transgenics · Animals · Cell Count · Cell Proliferation · Clone Cells · Encephalomyelitis, Autoimmune, Experimental · Epitopes · Female · Immune Tolerance · Immunization · Mannose · Mice · Peptides · Pertussis Toxin · Spleen · T-Lymphocytes · Mus

Abstract

Tolerance to experimental autoimmune encephalomyelitis (EAE) in SJL mice can be induced by immunization with a mannosylated form of the proteolipid protein (M-PLP139-151), despite the presence of CFA. The state of tolerance is characterized by poor delayed-type hypersensitivity responses and the absence of clinical EAE symptoms. In vivo monitoring of CFSE-labeled PLP139-151-specific TCR-transgenic (5B6) T cells revealed that immunization with M-PLP139-151 increases the clonal expansion of 5B6 T cells that do not develop full effector functions. Moreover, nonfunctional T cells obtained from M-PLP139-151-immunized mice showed poor blastogenesis and were unable to transfer EAE to naïve recipients. Nevertheless, the in vitro production of cytokines and chemokines associated with EAE was unaffected. Importantly, tolerance induced by M-PLP 139-151 was abrogated by the administration of pertussis toxin, resulting in EAE development. Our results suggest that M-PLP139-151 inhibits EAE development by affecting the differentiation of T cells into encephalitogenic effector cells. © Society for Leukocyte Biology.