High expression of interleukin-1β in the corneal epithelium of MRL/lpr mice is under the control of their genetic background

M. Okamoto, M. Takagi, M. Kutsuna, Y. Hara, M. Nishihara, M. C. Zhang, T. Matsuda, M. Sakanaka, S. Okamoto, M. Nose, Y. Ohashi

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8 Citations (Scopus)

Abstract

MRL/Mp mice bearing the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop polyarthritis, sialoadenitis and dacryoadenitis, resembling rheumatoid arthritis (RA), and also corneal involvement such as keratopathy and scleritis, which is a major complication in RA patients. In this study, we found that the expression levels of IL-1β and MMP-1 mRNAs in cornea were high in both MRL/lpr and MRL/Mp-+/+ strains of mice at an age younger than when they develop any inflammatory lesions. This was not true of other inbred strains, even those bearing the lpr gene, and also not of (NZB x NZW) F1 lupus mice. There was no significant difference in the expression of IL-1α and TGFβ in cornea in these strains. Using crosses between MRL/lpr and C3H/HeJ-lpr/lpr (C3H/lpr) mice, at least the expression of IL-1β was found to be under the control of the MRL genetic background, likely with a recessive mode of inheritance. Considering that IL-1β in cornea was detected particularly in the epithelial layer, the high expression of IL-1β in cornea is most likely involved in the genetic predisposition for corneal involvement and possibly also for arthritis in an MRL strain of mice.

Original languageEnglish
Pages (from-to)239-244
Number of pages6
JournalClinical and Experimental Immunology
Volume136
Issue number2
DOIs
Publication statusPublished - 2004 May

Keywords

  • Corneal ulcer
  • Genetic
  • IL-1α
  • MMP-1
  • Rheumatoid arthritis
  • TGFβ

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Okamoto, M., Takagi, M., Kutsuna, M., Hara, Y., Nishihara, M., Zhang, M. C., Matsuda, T., Sakanaka, M., Okamoto, S., Nose, M., & Ohashi, Y. (2004). High expression of interleukin-1β in the corneal epithelium of MRL/lpr mice is under the control of their genetic background. Clinical and Experimental Immunology, 136(2), 239-244. https://doi.org/10.1111/j.1365-2249.2004.02428.x