|
|
 Previous Article | Table of Contents | Next Article 
Blood, Vol. 94 No. 3 (August 1), 1999:
pp. 994-1002
T-Cell Receptor-Independent Activation of Clonal Th2 Cells
Associated With Chronic Hypereosinophilia
Florence Roufosse,
Liliane Schandené,
Catherine Sibille,
Bernard Kennes,
André Efira,
Elie Cogan, and
Michel Goldman
From the Departments of Immunology and Internal Medicine,
Hôpital Erasme, Université Libre de Bruxelles, Brussels;
the Institute of Pathology and Genetics, Loverval, Gerpinnes; the
Department of Internal Medicine, Centre Hospitalo-Universitaire
Vésale, Montigny le Tilleul; and the Department of Internal
Medicine, Hôpital St. Pierre, Université Libre de
Bruxelles, Brussels, Belgium.
We recently observed a clonal expansion of
CD3 CD4+ T cells secreting Th2-type
cytokines in patients presenting chronic hypereosinophilia. As clonal T
cells isolated from such patients did not spontaneously secrete
cytokines in vitro, we reasoned that costimulatory signals delivered by
antigen-presenting cells might be required to induce their full
activation. To address this question, we investigated in two such
patients the responses of CD3CD4+ T cells
to dendritic cells (DC). DC elicited proliferation and production of
interleukin-5 (IL-5) and IL-13 by clonal cells from patient 1 and
upregulated their expression of CD25 (IL-2R- ). These effects were
abolished when blocking monoclonal antibodies (MoAbs) against IL-2R-
and IL-2 were added to cocultures, indicating critical involvement of
an autocrine IL-2/IL-2R pathway. Cells from patient 2 were stimulated
by DC to produce Th2 cytokines only when rIL-2 or rIL-15 was added to
cocultures. In both patients, addition of inhibitory MoAbs against
B7-1/B7-2 or CD2 to cocultures resulted in dramatic reduction of
cytokine production and inhibited CD25 upregulation. Thus,
TCR/CD3-independent activation of clonal Th2 cells by DC is an
IL-2-dependent process, which requires signaling through CD2 and CD28.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
K. J. Smith, E. Jacobson, S. Hamza, and H. Skelton
Unexplained Hypereosinophilia and the Need for Cytogenetic and Molecular Genetic Analyses
Arch Dermatol,
May 1, 2004;
140(5):
584 - 588.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Gotlib, J. Cools, J. M. Malone III, S. L. Schrier, D. G. Gilliland, and S. E. Coutre
The FIP1L1-PDGFR{alpha} fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management
Blood,
April 15, 2004;
103(8):
2879 - 2891.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A M A. El-Asrar, S Struyf, S A Al-Kharashi, L Missotten, J Van Damme, and K Geboes
Expression of T lymphocyte chemoattractants and activation markers in vernal keratoconjunctivitis
Br. J. Ophthalmol.,
October 1, 2002;
86(10):
1175 - 1180.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Schandene, F. Roufosse, A. de Lavareille, P. Stordeur, A. Efira, B. Kennes, E. Cogan, and M. Goldman
Interferon alpha prevents spontaneous apoptosis of clonal Th2 cells associated with chronic hypereosinophilia
Blood,
December 15, 2000;
96(13):
4285 - 4292.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Bain
Eosinophilia -- Idiopathic or Not?
N. Engl. J. Med.,
October 7, 1999;
341(15):
1141 - 1143.
[Full Text]
|
|
|
|
|
