Wiskott-Aldrich syndrome protein deficiency in innate immune cells leads to mucosal immune dysregulation and colitis in mice

Deanna D Nguyen, Marc-Andre Wurbel, Jeremy A Goettel, Michelle A Eston, Osub S Ahmed, Romela Marin, Elisa K Boden, Eduardo J Villablanca, Helena Paidassi, Vineet Ahuja, Hans-Christian Reinecker, Edda Fiebiger, Adam Lacy-Hulbert, Bruce H Horwitz, J Rodrigo Mora, Scott B Snapper

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Immunodeficiency and autoimmune sequelae, including colitis, develop in patients and mice deficient in Wiskott-Aldrich syndrome protein (WASP), a hematopoietic cell-specific intracellular signaling molecule that regulates the actin cytoskeleton. Development of colitis in WASP-deficient mice requires lymphocytes; transfer of T cells is sufficient to induce colitis in immunodeficient mice. We investigated the interactions between innate and adaptive immune cells in mucosal regulation during development of T cell-mediated colitis in mice with WASP-deficient cells of the innate immune system.
Original languageEnglish
Pages (from-to)719-29.e1-2
JournalGastroenterology
Volume143
Issue number3
DOIs
Publication statusPublished - Sept 2012

Keywords / Materials (for Non-textual outputs)

  • Adoptive Transfer
  • Animals
  • Antigens, CD
  • Antigens, CD11b
  • CD4-Positive T-Lymphocytes
  • Cell Proliferation
  • Cells, Cultured
  • Colitis
  • Colon
  • DNA-Binding Proteins
  • Dendritic Cells
  • Disease Models, Animal
  • Forkhead Transcription Factors
  • Immune Tolerance
  • Immunity, Innate
  • Immunity, Mucosal
  • Integrin alpha Chains
  • Interleukin-10
  • Intestinal Mucosa
  • Lymphocyte Activation
  • Mice
  • Mice, 129 Strain
  • Mice, Knockout
  • T-Lymphocytes, Regulatory
  • Time Factors
  • Transplantation Chimera
  • Wiskott-Aldrich Syndrome Protein

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