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JCI online early table of contents: Sept. 19, 2011

EDITOR'S PICK: Link between ageing and Huntington disease provides candidate therapeutic target

Aging is a major risk factor for the progression of neurodegenerative diseases, including Huntington disease (HD). Morris White and colleagues, at Harvard Medical School, Boston, have now determined that modulating levels of the signaling protein Irs2 changes disease progression in a mouse model of HD. Specifically, increasing Irs2 levels in the brain increased nerve cell damage and reduced lifespan. Conversely, decreasing Irs2 levels reduced nerve cell damage, attenuated symptoms of disease, and increased lifespan. It has been previously shown that reducing Irs2 signaling increases the life span of mice; the data generated by White and colleagues suggests something more specific, that reducing IRS2 signaling could help slow the progression of HD.

TITLE: IRS2 increases mitochondrial dysfunction and oxidative stress in a mouse model of Huntington disease

Morris F. White
Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
Phone: 617.919.2846; Fax: 617.730.0244; E-mail:

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EDITOR'S PICK: High-calorie food 'looks' different to obese individuals

The number of individuals who are obese and suffer with its associated health problems has reached epidemic levels. One factor behind this is that we are constantly surrounded by high-calorie foods and/or images of these foods. Robert Sherwin and colleagues, at Yale University School of Medicine, New Haven, have now visualized differences in the way that the brains of obese and nonobese individuals respond to visual cues of high-calorie foods.

Sherwin and colleagues found that in nonobese individuals with low levels of glucose in their blood, certain regions of the brain were triggered in response to food cues and the individuals had a great desire for high-calorie foods. If these individuals had a normal level of glucose in their blood, different regions of the brain were triggered by the food cures and the individuals were less interested in high-calorie foods. Importantly, this ability of normal levels of glucose in the blood to reduce desire for high-calorie foods was not present in individuals who were obese.

TITLE: Circulating glucose levels modulate neural control of desire for high-calorie foods in humans

Robert S. Sherwin
Yale University School of Medicine, New Haven, Connecticut, USA.
Phone: 203.785.4183; Fax: 203.737.5558; E-mail:

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EDITOR'S PICK: Mast cells reduce toxicity of Gila monster and scorpion venom

Gila monsters are large venomous lizards. Although envenomation by the Gila monster is not often fatal to adult humans, it results in intense pain, swelling, weakness, and nausea. A team of researchers, led by Stephen Galli, at Stanford University School of Medicine, Stanford, has now uncovered a natural mechanism by which mice reduce the toxicity, and thereby the morbidity and mortality, of Gila monster venom immune cells known as mast cells release the protein MCPT4, which degrades the Gila monster venom helodermin. This mechanism also acted to reduce the toxicity of venom from 2 species of scorpions. These data provide insight into the benefits of mast cells, which have long been viewed as contributors to disease, in particular anaphylaxis and allergic diseases.

TITLE: Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice

Stephen J. Galli
Stanford University School of Medicine, Stanford, California, USA.
Phone: 650.723.7975; Fax: 650.725.6902; E-mail:

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IMMUNOLOGY: New genetic cause of Boy in the bubble syndrome

Severe combined immunodeficiency (SCID) is a rare but devastating genetic disorder sometimes known as 'Boy in the bubble syndrome', because the patient lacks one or more type of immune cell, making them very susceptible to infections. A team of researchers, led by Jos Regueiro, at Universidad Complutense, Spain, has now identified a new form of SCID characterized by a lack of just one particular T cell subset (those expressing a protein complex known as the alpha/beta TCR). Other immune cell types, including T cells expressing an alternative protein complex known as the gamma/delta TCR, were present in the affected individuals. The two patients with this condition were not in any way related but both had a leaky mutation in their two CD3D genes.

TITLE: A leaky mutation in CD3D differentially affects alpha/beta and gamma/delta T cells and leads to a T-alpha/beta−T-gamma/delta+B+NK+ human SCID

Jos R. Regueiro
Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Phone: 34913941642; Fax: 34913941641; E-mail:

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HIV/AIDS: B cells outFOXed by HIV

In most individuals, infection with HIV-1 leads to severe immune system deficiency. Much research has focused on the loss of immune cells known as CD4+ T cells that occurs, since these cells themselves can be infected with the virus. Much less is known about the profound deregulation of immune cells known as B cells, which are critical for riding the body of invading viruses through their production of molecules known as antibodies. A team of researchers, led by Elias Haddad and Rafick-Pierre Skaly, at the Vaccine and Gene Therapy Institute, Port St. Lucie, has now investigated this issue and identified a molecular mechanism responsible for the progressive depletion of a subset of B cells (specifically peripheral CD27+ memory B cells) in individuals chronically infected with HIV-1. This mechanism provides potential targets for enhancing B cell function, and thereby restoring antibody responses, including toward HIV-1, in individuals infected with HIV-1.

TITLE: Loss of memory B cells during chronic HIV infection is driven by Foxo3a- and TRAIL-mediated apoptosis

Elias K. Haddad
Vaccine and Gene Therapy Institute, Port St. Lucie, Florida, USA.
Phone: 772.971.5099; Fax: 772.345.3675; E-mail:

Rafick-Pierre Skaly
Vaccine and Gene Therapy Institute, Port St. Lucie, Florida, USA.
Phone: 772.345.4785; Fax: 772.345.3675; E-mail:

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IMMUNOLOGY: Genetic link to severe bacterial meningitis identifies potential therapeutic strategy

Meningitis is inflammation of the protective membranes covering the brain and spinal cord. When caused by bacteria it is a life-threatening condition. The most common cause of bacterial meningitis is Streptococcus pneumoniae, a condition known as pneumococcal meningitis. An inflammatory cascade known as the complement system has been implicated as a modulator of the severity of pneumococcal meningitis in animal models. A team of researchers, led by Diederik van de Beek, at Academic Medical Center, the Netherlands, has now identified a specific variant in the gene that templates the protein complement component 5 (C5) as being associated with poor outcome in individuals with bacterial meningitis. Further analysis in mice led the team to suggest that using immune molecules known as antibodies that target C5 could prove useful as a component of therapy for pneumococcal meningitis.

TITLE: Complement component 5 in humans and mice with pneumococcal meningitis

Diederik van de Beek
Academic Medical Center, Amsterdam, , NLD
Phone: +31 20 5664862; Fax: ; E-mail:

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TUMOR IMMUNOLOGY: Putting the heat on tumors

Immune cells have a key role in regulating tumor formation and progression some (such as CD8+ T cells) are key to restraining tumor formation and progression, while others actually promote these events. A team of researchers, led by Sharon Evans, at Roswell Park Cancer Institute, Buffalo, has now identified a way to enhance the movement of antitumor CD8+ T cells into tumors in mice. Specifically, the team defined a mechanism by which systemic thermal therapy (whereby the core temperature of the mice is elevated to 39.5C 0.5C for 6 hours) supported enhanced movement of CD8+ T cells into tumors. The hope is that these data can be exploited to create a therapeutic approach beneficial to individuals with cancer.

TITLE: IL-6 trans-signaling licenses mouse and human tumor microvascular gateways for trafficking of cytotoxic T cells

Sharon S. Evans
Roswell Park Cancer Institute, Buffalo, New York, USA.
Phone: 716.845.3421; Fax: 716.845.1322; E-mail:

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ONCOLOGY: Removing support for cancer cells

Pancreatic cancer is one of the most lethal cancers, with a 5-year survival rate of less than 5%. A team of researchers, led by Hideaki Ijichi, at the University of Tokyo, Japan, has now identified a new approach to reduce tumor progression in a mouse model of pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer in humans. Specifically, the team found that inhibiting the molecule Cxcr2 on the surface of stromal cells supporting the cancer cells reduced tumor progression and improved survival. The team therefore suggests that targeting tumor stromal cells, in particular by inhibiting Cxcr2, could provide a new approach for treating individuals with PDAC.

TITLE: Inhibiting Cxcr2 disrupts tumor-stromal interactions and improves survival in a mouse model of pancreatic ductal adenocarcinoma

Hideaki Ijichi
Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Phone: 81.3.3815.544; Fax: 81.3.3814.0021; E-mail:

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HEMATOLOGY: Triggering disease in a model of peripheral T cell lymphoma

Peripheral T cell lymphomas are a group of rare and usually aggressive lymphomas (cancers involving cells of the immune system). A team of researchers, led by Charles Roberts, at the Dana-Farber Cancer Institute, Boston, has identified in a mouse model of peripheral T cell lymphoma, the cell from which the lymphoma develops. In this model, the cell of origin a mature CD44hiCD122loCD8+ T cell resembled a subset of immune cells that has capacity for self-renewal and robust expansion, features shared with stem cells. Further analysis determined that signaling to CD44hiCD122loCD8+ T cells via a protein complex on their surface known as the TCR was required for the development of the lymphoma. Roberts and colleagues therefore suggest that targeting signals downstream of the TCR could provide a way to treat peripheral T cell lymphomas, which are usually hard to treat.

TITLE: TCR-dependent transformation of mature memory phenotype T cells in mice

Charles W.M. Roberts
Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Phone: 617.632.6497; Fax: 617.582.8096; E-mail:

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Contact: Karen Honey
Journal of Clinical Investigation

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