GATA2 regulates dendritic cell differentiation

Koichi Onodera, Tohru Fujiwara, Yasushi Onishi, Ari Itoh-Nakadai, Yoko Okitsu, Noriko Fukuhara, Kenichi Ishizawa, Ritsuko Shimizu, Masayuki Yamamoto and Hideo Harigae

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  • RE: Role for GATA-2 in adult hematopoiesis: response to Onodera et al.
    • Haiyan S. Li, Instructor MD Anderson Cancer Center
    • Other Contributors:
      • Stephanie S. Watowich, Professor

    Onodera et al. recently described a role for GATA-2 in dendritic cell (DC) differentiation 1. The data agree closely with our published results 2. Nonetheless, we reached a distinct conclusion: GATA-2 is critical to maintain c-Kit on hematopoietic progenitors 2. We suggest this is a common mechanism for phenotypes reported in both manuscripts. Each study used conditional Gata2 deletion driven by ubiquitously expressed tamoxifen-inducible CreER 1,2. We additionally employed bone marrow transplantation to delineate hematopoietic-intrinsic Gata2 function 2. Upon Gata2 removal, we observed rapid loss of bone marrow, spleen and thymic cellularity, with peripheral cytopenia. Myeloid populations were sensitive to Gata2-deficiency, yet we also observed significant reduction in DCs and lymphocytes, as well as decreased c-Kit on hematopoietic progenitors 2. Molecular studies and enforced c-Kit expression in Gata2-deficient progenitors indicated an intrinsic role for GATA-2 in Kit regulation and progenitor function 2. By contrast, Onodera et al. suggest GATA-2 directs myeloid versus T lymphocyte specification in DC progenitors, thereby regulating the myeloid pathway of DC differentiation. This is counter to current understanding of DCs arising from common Flt3-positive progenitors 3. Additionally, they report deficiencies in other myeloid populations as well as hematopoietic progenitors defined by c-Kit expression 1. Since phenotypic marker assays were used to assess progenitors 1, p...

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    Conflict of Interest:
    None declared.