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2016 ; 7
(ä): 330
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Hematopoietic Stem Cell Regulation by Type I and II Interferons in the
Pathogenesis of Acquired Aplastic Anemia
#MMPMID27621733
Smith JN
; Kanwar VS
; MacNamara KC
Front Immunol
2016[]; 7
(ä): 330
PMID27621733
show ga
Aplastic anemia (AA) occurs when the bone marrow fails to support production of
all three lineages of blood cells, which are necessary for tissue oxygenation,
infection control, and hemostasis. The etiology of acquired AA is elusive in the
vast majority of cases but involves exhaustion of hematopoietic stem cells (HSC),
which are usually present in the bone marrow in a dormant state, and are
responsible for lifelong production of all cells within the hematopoietic system.
This destruction is immune mediated and the role of interferons remains
incompletely characterized. Interferon gamma (IFN?) has been associated with AA
and type I IFNs (alpha and beta) are well documented to cause bone marrow aplasia
during viral infection. In models of infection and inflammation, IFN? activates
HSCs to differentiate and impairs their ability to self-renew, ultimately leading
to HSC exhaustion. Recent evidence demonstrating that IFN? also impacts the HSC
microenvironment or niche, raises new questions regarding how IFN? impairs HSC
function in AA. Immune activation can also elicit type I interferons, which may
exert effects both distinct from and overlapping with IFN? on HSCs. IFN?/?
increase HSC proliferation in models of sterile inflammation induced by
polyinosinic:polycytidylic acid and lead to BM aplasia during viral infection.
Moreover, patients being treated with IFN? exhibit cytopenias, in part due to BM
suppression. Herein, we review the current understanding of how interferons
contribute to the pathogenesis of acquired AA, and we explore additional
potential mechanisms by which interferons directly and indirectly impair HSCs. A
comprehensive understanding of how interferons impact hematopoiesis is necessary
in order to identify novel therapeutic approaches for treating AA patients.
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