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Do, Yoonkyung
DC-based Immune System & Immunotherapy (DISNI) Lab
Research Interests
  • Study on various subsets of dendritic cells and their immunological functions

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Combined deficiency in CD44 and Fas leads to exacerbation of lymphoproliferative and autoimmune disease

Cited 7 times inthomson ciCited 9 times inthomson ci
Title
Combined deficiency in CD44 and Fas leads to exacerbation of lymphoproliferative and autoimmune disease
Author
Do, YoonkyungRafi-Janajreh, AQMckallip, RJNagarkatti, PSNagarkatti, M
Keywords
Activation-induced cell death; Apoptosis; Autoantibody; Double-negative T cells; Lupus
Issue Date
200311
Publisher
OXFORD UNIV PRESS
Citation
INTERNATIONAL IMMUNOLOGY, v.15, no.11, pp.1327 - 1340
Abstract
Patients with mutations in Fas develop autoimmune lymphoproliferative disease (ALPS), While their family members with similar mutations are often normal, thereby suggesting that additional factors may play a role in the development of ALPS. In the current study, we tested the role of CD44 in the development of lymphoproliferative disease by generating CD44 -/-/Fas -/-mice, which failed to express CD44 and Fas, and compared them to CD44 +/+/Fas -/- mice that expressed CD44, but not Fas. The results showed that CD44 -/-/Fas -/- mice developed a more severe lymphoproliferative and autoimmune disease when compared to CD44 +/+/Fas -/- mice. This was indicated by increased numbers of cells in their lymph nodes, and a greater proportion of B220 +CD4 -CD8 - (double-negative) T cells as well as antibodies against single-stranded DNA and chromatin. The heightened severity of lymphoproliferative disease seen in CD44 -/-/Fas -/- mice correlated with increased resistance of T cells, but not B cells, to undergo activation-induced cell death (AICD). The current study suggests that deficiency in CD44 in combination with a defect in one of the molecules involved in the death receptor family such as Fas can further down-regulate AICD, and exacerbate the lymphoproliferative and autoimmune disease.
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DOI
http://dx.doi.org/10.1093/intimm/dxg132
ISSN
0953-8178
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SLS_Journal Papers

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