L-Selectin-deficient SJL and C57BL/6 mice are not resistant to experimental autoimmune encephalomyelitis

Chiara Uboldi, Axinia Döring, Carsten Alt, Pila Estess, Mark Siegelman, Britta Engelhardt

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

L-selectin has been suggested to play a role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Here we demonstrate that L-selectin-/- SJL mice are susceptible to proteolipid protein (PLP)-induced EAE because the compromised antigen-specific T cell proliferation in peripheral lymph nodes is fully compensated by the T cell response raised in their spleen. Transfer of PLP-specific T cells into syngeneic recipients induced EAE independent of the presence or absence of L-selectin on PLP-specific T cells or in the recipient. Leukocyte infiltration into the central nervous system parenchyma was detectable independent of the mode of disease induction and the presence or absence of L-selectin. In addition, we found L-selectin-/- C57BL/6 mice to be susceptible to myelin oligodendrocyte glycoprotein-induced EAE. Taken together, we demonstrate that in SJL and C57BL/6 mice L-selectin is not required for EAE pathogenesis. The apparent discrepancy of our present observation to previous findings, demonstrating a role of L-selectin in EAE pathogenesis in C57BL/6 mice or myelin-basic protein (MBP)-specific TCR-transgenic B10.PL mice, may be attributed to background genes rather than L-selectin and to a unique role of L-selectin in EAE pathogenesis in MBP-TCR-transgenic mice.

Original languageEnglish (US)
Pages (from-to)2156-2167
Number of pages12
JournalEuropean Journal of Immunology
Volume38
Issue number8
DOIs
StatePublished - Aug 2008

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Keywords

  • C57BL/6 mouse
  • Experimental autoimmune encephalomyelitis
  • L-Selection SJL mouse
  • Lymphocyte trafficking

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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