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Blood, 1 March 2002, Vol. 99, No. 5, pp. 1610-1619
HEMATOPOIESIS
Bone marrow progenitor cell reserve and function and stromal cell
function are defective in rheumatoid arthritis: evidence for a tumor
necrosis factor alpha-mediated effect
Helen A. Papadaki,
Heraklis
D. Kritikos,
Claudia Gemetzi,
Helen Koutala,
Judith C. W. Marsh,
Dimitrios T. Boumpas, and
George D. Eliopoulos
From the Departments of Hematology and Rheumatology,
University Hospital of Crete School of Medicine, Heraklion, Greece; and
the Department of Hematology, St George's Hospital Medical School,
London, United Kingdom.
Based on previous reports for impaired hematopoiesis in rheumatoid
arhrtitis (RA), and in view of the current interest in exploring the
role of autologous stem cell transplantation (ASCT) as an alternative
treatment in patients with resistant disease, we have evaluated bone
marrow (BM) progenitor cell reserve and function and stromal cell
function in 26 patients with active RA. BM progenitor cells were
assessed using flow cytometry and clonogenic assays in short-term and
long-term BM cultures (LTBMCs). BM stroma function was assessed by
evaluating the capacity of preformed irradiated LTBMC stromal layers to
support the growth of normal CD34+ cells. We found that RA
patients exhibited low number and increased apoptosis of
CD34+ cells, defective clonogenic potential of BM
mononuclear and purified CD34+ cells, and low progenitor
cell recovery in LTBMCs, compared with healthy controls (n = 37).
Patient LTBMC stromal layers failed to support normal hematopoiesis and
produced abnormally high amounts of tumor necrosis factor alpha
(TNF ). TNF levels in LTBMC supernatants inversely correlated with
the proportion of CD34+ cells and the number of
colony-forming cells, and positively with the percentage of
apoptotic CD34+ cells. Significant restoration of the
disturbed hematopoiesis was obtained following anti-TNF treatment in
12 patients studied. We concluded that BM progenitor cell reserve and
function and BM stromal cell function are defective in RA probably due,
at least in part, to a TNF-mediated effect. The role of these
abnormalities on stem cell harvesting and engraftment in RA patients
undergoing ASCT remains to be clarified.
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