CD1d deficiency exacerbates inflammatory dermatitis in MRL-lpr/lpr mice

Jun Qi Yang, Taehoon Chun, Hongzhu Liu, Seokmann Hong, Hai Bui, Luc Van Kaer, Chyung Ru Wang, Ram Raj Singh

Research output: Contribution to journalArticlepeer-review

52 Citations (Scopus)

Abstract

Mechanisms responsible for the development of autoimmune skin disease in humans and animal models with lupus remain poorly understood. In this study, we have investigated the role of CD1d, an antigen-presenting molecule known to activate natural killer T cells, in the development of inflammatory dermatitis in lupus-susceptible MRL-lpr/lpr mice. In particular, we have established MRL-lpr/lpr mice carrying a germ-line deletion of the CD1d genes. We demonstrate that CD1d-deficient MRL-lpr/lpr mice, as compared with wild-type littermates, have more frequent and more severe skin disease, with increased local infiltration with mast cells, lymphocytes and dendritic cells, including Langerhans cells. CD1d-deficient MRL-lpr/lpr mice had increased prevalence of CD4+ T cells in the spleen and liver and of TCRαβ+B220+ cells in lymph nodes. Furthermore, CD1d deficiency was associated with decreased T cell production of type 2 cytokines and increased or unchanged type 1 cytokines. These findings indicate a regulatory role of CD1d in inflammatory dermatitis. Understanding the mechanisms by which CD1d deficiency results in splenic T cell expansion and cytokine alterations, with increased dermal infiltration of dendritic cells and lymphocytes in MRL-lpr/lpr mice, will have implications for the pathogenesis of inflammatory skin diseases.

Original languageEnglish
Pages (from-to)1723-1732
Number of pages10
JournalEuropean Journal of Immunology
Volume34
Issue number6
DOIs
Publication statusPublished - 2004 Jun

Keywords

  • Autoimmunity
  • CD1d
  • Dermatitis
  • Lupus
  • NKT cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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