Regulatory lymphocytes are key factors in mhc-independent resistance to EAE

Nieves Marín, Miriam Mecha, Carmen Espejo, Leyre Mestre, Herena Eixarch, Xavier Montalban, José C. Álvarez-Cermeño, Carmen Guaza, Luisa M. Villar

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)

Abstract

Background and Objectives. Resistant and susceptible mouse strains to experimental autoimmune encephalomyelitis (EAE), an inducible demyelinating experimental disease serving as animal model for multiple sclerosis, have been described. We aimed to explore MHC-independent mechanisms inducing resistance to EAE. Methods. For EAE induction, female C57BL/6 (susceptible strain) and CD1 (resistant outbred strain showing heterogeneous MHC antigens) mice were immunized with the 35-55 peptide of myelin oligodendrocyte glycoprotein (MOG35-55). We studied T cell proliferation, regulatory and effector cell subpopulations, intracellular and serum cytokine patterns, and titers of anti-MOG serum antibodies. Results. Upon immunization with MOG35-55, T lymphocytes from susceptible mice but not that of resistant strain were capable of proliferating when stimulated with MOG35-55. Accordingly, resistant mice experienced a rise in regulatory B cells (P = 0.001) and, to a lower extent, in regulatory T cells (P = 0.02) compared with C57BL/6 susceptible mice. As a consequence, MOG35-55-immunized C57BL/6 mice showed higher percentages of CD4+ T cells producing both IFN-gamma (P = 0.02) and IL-17 (P = 0.009) and higher serum levels of IL-17 (P = 0.04) than resistant mice. Conclusions. Expansion of regulatory B and T cells contributes to the induction of resistance to EAE by an MHC-independent mechanism. © 2014 Nieves Marín et al.
Original languageEnglish
Article number156380
JournalJournal of Immunology Research
Volume2014
DOIs
Publication statusPublished - 1 Jan 2014

Fingerprint Dive into the research topics of 'Regulatory lymphocytes are key factors in mhc-independent resistance to EAE'. Together they form a unique fingerprint.

Cite this