Dendritic cell-MHC class II and Itk regulate functional development of regulatory innate memory CD4+ T cells in bone marrow transplantation

Weishan Huang, Qian Qi, Jianfang Hu, Fei Huang, Terri M. Laufer, Avery August

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

MHC class II (MHCII)-influenced CD4+ T cell differentiation and function play critical roles in regulating the development of autoimmunity. The lack of hematopoietic MHCII causes autoimmune disease that leads to severe wasting in syngeneic recipients. Using murine models of bone marrow transplantation (BMT), we find that MHCII-/-→wild-type BMT developed disease, with defective development of innate memory phenotype (IMP, CD44hi/CD62Llo) CD4+ T cells. Whereas conventional regulatory T cells are unable to suppress pathogenesis, IMP CD4+ T cells, which include conventional regulatory T cells, can suppress pathogenesis in MHCII-/-→wild-type chimeras. The functional development of IMP CD4+ T cells requires hematopoietic but not thymic MHCII. B cells and hematopoietic CD80/86 regulate the population size, whereas MHCII expression by dendritic cells is sufficient for IMP CD4+ T cell functional development and prevention of pathogenesis. Furthermore, the absence of Tec kinase IL-2-inducible T cell kinase in MHCII-/- donors leads to preferential development of IMP CD4+ T cells and partially prevents pathogenesis. We conclude that dendritic cells-MHCII and IL-2-inducible T cell kinase regulate the functional development of IMP CD4+ T cells, which suppresses the development of autoimmune disorder in syngeneic BMTs. The Journal of Immunology, 2014, 192: 3435.3441.

Original languageEnglish (US)
Pages (from-to)3435-3441
Number of pages7
JournalJournal of Immunology
Volume192
Issue number7
DOIs
StatePublished - Apr 1 2014

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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