|
|
 Previous Article | Table of Contents | Next Article 
Blood, 15 August 2001, Vol. 98, No. 4, pp. 966-971
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
The nonexpression of CD36 on reticulocytes and mature red blood
cells does not modify the clinical course of patients with sickle
cell anemia
Ketty Lee,
Pierre Gane,
Françoise Roudot-Thoraval,
Bertand Godeau,
Dora Bachir,
Françoise Bernaudin,
Jean-Pierre Cartron,
Frédéric Galactéros, and
Philippe Bierling
From the EFS-Ile de France, Laboratoire d'immunologie
leuco-plaquettaire; the Unité d'évaluation-études;
the Service de médecine interne; and the Unité de
génétique médicale, Hôpital Henri Mondor,
AP-HP, Créteil; the Service de pédiatrie, center
hospitalier intercommunal de Créteil; and INSERM U76, INTS,
Paris, France.
It is thought that an increase in the adhesion of circulating
reticulocytes to the vascular endothelium may initiate the vascular occlusion underlying the painful crises and organ failures typical of
sickle cell disease (SCD). At least 2 receptors, usually present on
reticulocytes, seem to be involved in this adhesion process: glycoprotein CD36 (glycoprotein IV) and integrin
 4 1 (very late activation
antigen-4). Recently, a high frequency of the platelet CD36-deficient phenotype was reported in black Africans. The
frequency of this deficiency was similar in subjects with and without
SCD. The role of CD36 in vaso-occlusion was then investigated by
comparing the clinical course in 2 groups of black Africans homozygous
for hemoglobin S, with and without CD36 deficiency, but similar in age,
sex, geographical origin, number of -globin genes, and -globin gene haplotype. Flow cytometry showed that CD36 was absent from the
circulating red blood cells and reticulocytes of platelet CD36-deficient individuals but present on those from patients with
normal platelet CD36 expression, and that
41 integrin levels were similar on the
reticulocytes of the 2 groups. Neither clinical severity, as evaluated
by the frequency and characteristics of vaso-occlusive events, nor
biological data differed significantly in the 2 groups of patients.
Finally, although CD36 has been suggested to play a critical role in
the pathogenesis of vaso-occlusion, this study, despite including only
a small number of patients, supports the idea that the modulation of
expression of a single type of adhesion molecule is insufficient to
counteract the pathological process leading to vaso-occlusion in SCD patients.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
M.-H. Odievre, V. Bony, M. Benkerrou, C. Lapoumeroulie, C. Alberti, R. Ducrocq, E. Jacqz-Aigrain, J. Elion, and J.-P. Cartron
Modulation of erythroid adhesion receptor expression by hydroxyurea in children with sickle cell disease
Haematologica,
April 1, 2008;
93(4):
502 - 510.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. El Nemer, M.-P. Wautier, C. Rahuel, P. Gane, P. Hermand, F. Galacteros, J.-L. Wautier, J.-P. Cartron, Y. Colin, and C. Le Van Kim
Endothelial Lu/BCAM glycoproteins are novel ligands for red blood cell {alpha}4{beta}1integrin: role in adhesion of sickle red blood cells to endothelial cells
Blood,
April 15, 2007;
109(8):
3544 - 3551.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. M. Matsui, A. Varki, and S. H. Embury
Heparin inhibits the flow adhesion of sickle red blood cells to P-selectin
Blood,
November 15, 2002;
100(10):
3790 - 3796.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. N. Y. Setty, S. Kulkarni, and M. J. Stuart
Role of erythrocyte phosphatidylserine in sickle red cell-endothelial adhesion
Blood,
March 1, 2002;
99(5):
1564 - 1571.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
