NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 27 November 2005
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
* Summaries of newsworthy papers:
* Visualizing suppression of autoimmune disease - Nature Immunology
* Polycystic kidney disease unravelled - Nature Cell Biology
* Mention of papers to be published at the same time with the same embargo
* Geographical listing of authors
PDFs of all the papers mentioned on this release can be found in the
relevant journal's section of http://press.nature.com. Press contacts for
the Nature journals are listed at the end of this release.
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***************************NATURE IMMUNOLOGY*****************************
(<http://www.nature.com/natureimmunology>)
[1] Visualizing suppression of autoimmune disease
DOI: 10.1038/ni1289
Scientists have devised a way to view how autoimmunity is averted, as
reported in the January issue of Nature Immunology. Jeffrey Bluestone and
colleagues have used a new technique called two-photon laser-scanning
microscopy to directly visualize immune cells at work inside the body.
Interactions between regulatory T cells (or Treg cells) and specialized
antigen-presenting cells prove to be key in preventing autoimmunity.
How our immune system avoids attacking healthy tissues has been a
longstanding issue in immunology. Scientists discovered that a population of
immune cells called Treg cells can prevent rogue autoimmune cells from
attacking self tissues, yet the targets of Treg cell action have remained
unclear. Using a mouse model of diabetes, these authors show that Treg cells
interact directly with antigen-presenting cells in draining pancreatic lymph
nodes. In the absence of Treg cells, potentially pathogenic autoreactive T
cells swarm around the antigen-presenting cells, picking up cues to attack
even their own tissues. This immune cell education process is called
'priming'. Like a traffic cop, however, the Treg cells keep them moving.
Notably, the Treg cells do not contact the autoreactive T cells directly.
Instead, they somehow modify the antigen-presenting cells, lessening the
chances for priming of the autoimmune cells. What exactly Treg cells do to
the antigen-presenting cells is still unknown.
This study lends support to the idea that antigen-presenting cells are
critical for Treg cell function and suggests that direct interaction between
Treg cells and autoreactive T cells is not required, as has been previously
suggested.
Author contact:
Jeffrey A Bluestone (University of California, San Francisco, CA, USA)
Tel: + 1 415 514 1683; E-mail: [email protected]
<mailto:[email protected]>
Other papers from Nature Immunology to be published online at the same time
and with the same embargo:
[2] Suppressor of cytokine signaling 1 regulates the immune response to
infection by a unique inhibition of type I interferon activity
DOI: 10.1038/ni1287
[3] Impaired assembly of the major histocompatibility complex MHC class I
peptide-loading complex in mice deficient in the oxidoreductase ERp57
DOI: 10.1038/ni1288
*************************NATURE CELL BIOLOGY**************************
(<http://www.nature.com/naturecellbiology>)
[4] Polycystic kidney disease unravelled
DOI: 10.1038/ncb1326
The catastrophic consequences of autosomal dominant polycystic kidney
disease (ADPKD), are caused by two mutated genes working together to cause
abnormal cell proliferation that ultimately leads to renal failure. New
results published by Jing Zhou and colleagues in the December issue of
Nature Cell Biology unravel how these mutated genes operate. ADPKD is a
hereditary affliction of the kidney affecting 1 in 1000 people.
ADPKD is caused by mutation of either the PC1 or the PC2 gene. These are
membrane proteins that interact, and may form a signalling receptor and ion
channel complex. Several signalling pathways are influenced by the PC1-PC2
complex, but it has remained unclear how mutation of these genes leads to
derailed renal epithelial cell proliferation.
The Zhou group now demonstrates that PC2 associates with the important cell
cycle and cell differentiation regulatory protein, Id2. This association
prevents entry of Id2 into the cell nucleus, where it normally acts on cell
cycle genes. PC1 turns out to be essential for the PC2-Id2 interaction,
explaining why loss of either PC1 or PC2 leads to unchecked nuclear
accumulation, and therefore derailed activation of the growth promoter Id2,
in the kidney cells of ADPKD patients. Reduced Id2 expression in cells from
a mouse model of ADPKD normalizes cell proliferation, although it remains to
be seen if this prevents further kidney disease. Nevertheless, these data
suggest that Id2 inhibition is a promising line of therapeutic intervention
for this common and severe kidney disease.
Author contact:
Jing Zhou (Brigham and Women's Hospital and Harvard Medical School, Boston,
MA, USA)
Tel: + 1 617 525 5860; E-mail: [email protected]
*******************************************************************
Items from other Nature journals to be published online at the same time and
with the same embargo:
Nature CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[5] Direct transfer of extended groups from synthetic cofactors by DNA
methyltransferases
DOI: 10.1038/nchembio754
Nature MEDICINE (http://www.nature.com/naturemedicine)
[6] Trans-arachidonic acids generated during nitrative stress induce a
thrombospondin-1-dependent microvascular degeneration
DOI: 10.1038/nm1336
[7] A role for LEDGF/p75 in targeting HIV DNA integration
DOI: 10.1038/nm1329
[8] Regression of abdominal aortic aneurysm by inhibition of c-Jun
N-terminal kinase
DOI: 10.1038/nm1335
[9] Acute rejection is associated with antibodies to non-Gal antigens in
baboons using Gal-knockout pig kidneys
DOI: 10.1038/nm1330
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)
[10] Induction and monitoring of definitive and visceral endoderm
differentiation of mouse ES cells
DOI: 10.1038/nbt1167
[11] Identification of post-translational modifications by blind search of
mass spectra
DOI: 10.1038/nbt1168
NATURE GENETICS (http://www.nature.com/naturegenetics)
[12] Lymphoid cell growth and transformation are suppressed by a key
regulatory element of the gene encoding PU.1
DOI: 10.1038/ng1679
[13] Identification of the gene responsible for methylmalonic aciduria and
homocystinuria, cblC type
DOI: 10.1038/ng1683
[14] Oral-facial-digital type I protein is required for primary cilia
formation and left-right axis specification
DOI: 10.1038/ng1684
[15] A positive signal from the fertilization of the egg cell sets off
endosperm proliferation in angiosperm embryogenesis
DOI: 10.1038/ng1694
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[16] Neuronal glutathione deficiency and age-dependent neurodegeneration in
the EAAC1 deficient mouse
DOI: 10.1038/nn1609
[17] ORL1 receptor-mediated internalization of N-type calcium channels
DOI: 10.1038/nn1605
[18] Classical and operant conditioning differentially modify the intrinsic
properties of an identified neuron
DOI: 10.1038/nn1593
[19] Sensorimotor attenuation by central motor command signals in the
absence of movement
DOI: 10.1038/nn1592
****************************************************************
GEOGRAPHICAL LISTING OF AUTHORS
The following list of places refers to the whereabouts of authors on the
papers numbered in this release. The listing may be for an author's main
affiliation, or for a place where they are working temporarily. Please see
the PDF of the paper for full details.
AUSTRALIA
Clayton: 2
Fitzroy: 2
Parkville: 2
CANADA
Calgary: 1, 13, 17
London: 6, 17
Melbourne: 2
Montreal: 6, 13
Sherbrooke: 6
Toronto: 4, 13
CHINA
Kunming: 9
Wuhan: 9
FRANCE
Illkirch: 14
Montpellier: 17
Paris: 6
GERMANY
Aachen: 5
Berlin: 12
Cologne: 15
Hannover: 12
Heidelberg: 3
ITALY
Naples: 14
JAPAN
Kobe: 10
Kyoto: 10
Sapporo: 3
Ube: 8
LITHUANIA
Vilnius: 6
NORWAY
Oslo: 15
SWITZERLAND
Zurich: 8
UNITED KINGDOM
London: 19
UNITED STATES OF AMERICA
California
La Jolla: 7, 11
Los Angeles: 11
San Francisco: 1, 16
Massachusetts
Boston: 4, 12
Minnesota
Rochester: 7
Missouri
St. Louis: 2
New York
Valhalla: 6
Ohio
Columbus: 12
Pennsylvania
Philadelphia: 7
Pittsburgh: 9
Texas
Dallas: 6
Houston: 18
Virginia
Blacksburg: 9
Charlottesville: 4
PRESS CONTACTS...
For media inquiries relating to embargo policy for all the Nature Research
Journals:
Katharine Mansell (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]
For media inquiries relating to editorial content/policy for the Nature
Research Journals, please contact the journals individually:
Nature Biotechnology (New York)
Kathy Aschheim
Tel: +1 212 726 9346; E-mail: [email protected]
Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]
Nature Chemical Biology (Boston)
Beatrice Chrystall
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Ed Feng
Tel: +1 212 726 9351; E-mail: [email protected]
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