|
|
Prepublished online as a Blood First Edition Paper on December 27, 2002; DOI 10.1182/blood-2002-06-1855.
 Previous Article | Table of Contents | Next Article 
Blood, 1 May 2003, Vol. 101, No. 9, pp. 3550-3559
IMMUNOBIOLOGY
Promoter IV of the class II transactivator gene is essential
for positive selection of CD4+ T cells
Jean-Marc Waldburger,
Simona Rossi,
Georg A. Hollander,
Hans-Reimer Rodewald,
Walter Reith, and
Hans Acha-Orbea
From the Institute of Biochemistry and Ludwig
Institute for Cancer Research, Lausanne Branch, University of Lausanne,
Epalinges, Switzerland; Department of Genetics and
Microbiology, University of Geneva, Medical School, Geneva,
Switzerland; Pediatric Immunology, Departments of Research
and Clinical-biological Sciences, and the Children's Hospital,
University of Basel, Switzerland; Department for
Immunology, University Clinics Ulm, Germany.
Major histocompatibility complex class II (MHCII)
expression is regulated by the transcriptional coactivator CIITA.
Positive selection of CD4+ T cells is abrogated in mice
lacking one of the promoters (pIV) of the Mhc2ta gene. This
is entirely due to the absence of MHCII expression in thymic epithelia,
as demonstrated by bone marrow transfer experiments between wild-type
and pIV / mice. Medullary thymic epithelial cells
(mTECs) are also MHCII in pIV/ mice.
Bone marrow-derived, professional antigen-presenting cells (APCs)
retain normal MHCII expression in pIV/ mice, including
those believed to mediate negative selection in the thymic medulla.
Endogenous retroviruses thus retain their ability to sustain negative
selection of the residual CD4+ thymocytes in
pIV/ mice. Interestingly, the passive acquisition of
MHCII molecules by thymocytes is abrogated in pIV/
mice. This identifies thymic epithelial cells as the source of this
passive transfer. In peripheral lymphoid organs, the CD4+
T-cell population of pIV/ mice is quantitatively and
qualitatively comparable to that of MHCII-deficient mice. It comprises
a high proportion of CD1-restricted natural killer T cells,
which results in a bias of the V repertoire of the residual
CD4+ T-cell population. We have also addressed the identity
of the signal that sustains pIV expression in cortical epithelia. We found that the Jak/STAT pathways activated by the common  chain (CD132) or common chain (CDw131) cytokine receptors are not required for MHCII expression in thymic cortical epithelia.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
S. Zuklys, J. Gill, M. P. Keller, M. Hauri-Hohl, S. Zhanybekova, G. Balciunaite, K.-J. Na, L. T. Jeker, K. Hafen, N. Tsukamoto, et al.
Stabilized {beta}-Catenin in Thymic Epithelial Cells Blocks Thymus Development and Function
J. Immunol.,
March 1, 2009;
182(5):
2997 - 3007.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Ngo, K. Patel, P. G Isaacson, and K. N Naresh
Leucocyte common antigen (CD45) and CD5 positivity in an "undifferentiated" carcinoma: a potential diagnostic pitfall
J. Clin. Pathol.,
August 1, 2007;
60(8):
936 - 938.
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Yao, Q. Xu, M.-J. Kwon, R. Matta, Y. Liu, S.-C. Hong, and C.-H. Chang
ERK and p38 MAPK Signaling Pathways Negatively Regulate CIITA Gene Expression in Dendritic Cells and Macrophages
J. Immunol.,
July 1, 2006;
177(1):
70 - 76.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
