Open AccessVaccinia Virus Infection Modulates the Hematopoietic Cell Compartments in the Bone Marrow
Author(s) -
Singh Pratibha,
Yao Yongxue,
Weliver Abigail,
Broxmeyer Hal E.,
Hong SoonCheol,
Chang CheongHee
Publication year - 2008
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1634/stemcells.2007-0461
Subject(s) - biology , haematopoiesis , progenitor cell , immune system , bone marrow , myeloid , immunology , stem cell , population , microbiology and biotechnology , demography , sociology
Successful proliferation and differentiation of hematopoietic progenitor cells in bone marrow (BM) is essential to generate all mature blood cell types, including those involved in the immune response. Although vaccinia virus (VV) is known to induce a strong immune response, the effect of VV infection on hematopoiesis remains largely unknown. Here, we showed that in vivo VV infection results in the expansion of c‐Kit hi Sca‐1 + Lin − (KSL) hematopoietic stem cells. The in vivo expansion of the KSL population requires MyD88 that is a critical adaptor for Toll‐like receptor‐mediated signaling. Moreover, in BM of VV‐infected mice, common myeloid progenitors (CMP) was decreased because of the rapid differentiation of CMP to more mature cells. However, the CMP compartment was not affected by VV infection in the absence of MyD88. The common lymphoid progenitor (CLP) cell population was increased regardless of MyD88 status, suggesting the independent regulation of CMP and CLP compartments by VV infection. VV infection also enhanced the potential of progenitors that preferentially induce the programming of dendritic cell (DC) development toward plasmacytoid DC. Therefore, the host immune response is gearing toward antiviral responses as early as at the precursor level upon VV infection. Disclosure of potential conflicts of interest is found at the end of this article.