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JCI early table of contents for Feb. 10, 2014

JCI Journals

Researchers identify unique regulatory T cell population in human skin

Regulatory T cells (Tregs) dampen the immune response against self antigens and contribute to the prevention of autoimmunity. A skin-specific population of Tregs (mTreg) has been described in mice that has properties similar to memory T cells. In mice, some mTregs are maintained in the skin for long periods of time and suppress cutaneous autoimmunity. In this issue of the Journal of Clinical Investigation, Michael Rosenblum and colleagues at the University of California San Francisco analyzed the mTreg population in human skin, and found that human mTregs have unique features and localize to hair follicles. mTregs isolated from human skin did not appear to recognize the same antigens as memory T cells isolated from blood. In healthy skin, mTregs were relatively static; however, this population was greatly expanded in skin from psoriasis patients, suggesting that these cells are dysfunctional in inflamed skin.

TITLE: Memory regulatory T cells reside in human skin

AUTHOR CONTACT: Michael D. Rosenblum
UCSF, San Francisco, CA, USA
Phone: +14153537800; E-mail:

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Familial amyotrophic lateral sclerosis-associated mutation damages DNA and alters RNA splicing

Familial amyotrophic lateral sclerosis (FALS) is a neurological disease that has been linked to mutations in several different genes, including the gene encoding the DNA/RNA binding protein FUS. It is unclear how FUS mutations promote FALS-associated symptoms. In the issue of the Journal of Clinical Investigation, Eric Huang and colleagues of the University of California San Francisco developed a transgenic mouse model of FUS-associated FALS. FUS-R521C mice exhibited phenotypes similar to patients, such as neurological dysfunction and pronounced DNA damage. The authors identified brain-derived neurotrophic factor (Bdnf) as a target of mutant FUS. Treatment of FUS-R521C neurons with BNDF only partially restored dendrite function. Evaluation of spinal cords from FUS-R521C revealed that there were multiple defects in the transcription and splicing of genes associated with dendrite growth and function.

TITLE: ALS-associated mutation FUS-R521C causes DNA damage and RNA splicing defects

University of California San Francisco UCSF, San Francisco, CA, USA
Phone: 415-476-8525; Fax: 415-514-0878; E-mail:

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TITLE: Optogenetic stimulation of the auditory pathway

University Medical Center Göttingen, Göttingen, , DEU
Phone: 551-39-8968; E-mail:

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TITLE: B cells mediate chronic allograft rejection independently of antibody production

AUTHOR CONTACT: Geetha Chalasani
University of Pittsburgh, Pittsburgh, PA, USA
Phone: (412) 383-5924; Fax: (412) 383-9990; E-mail:

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TITLE: 5′RNA-Seq identifies Fhl1 as a genetic modifier in cardiomyopathy

AUTHOR CONTACT: Christine Edry Seidman
Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA
Phone: 617-432-7838; Fax: 617-432-7832; E-mail:

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TITLE: CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis

AUTHOR CONTACT: Stefan Kaufmann
Max Planck Institute for Infection Biology, Berlin, , DEU

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TITLE: IL-15 regulates memory CD8+ T cell O-glycan synthesis and affects trafficking

University of Iowa, Iowa City, IA, USA
Phone: 319-335-9720; Fax: 319-335-9006;

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TITLE: An AXL/LRP-1/RANBP9 complex mediates DC efferocytosis and antigen cross-presentation in vivo

Rm PH 8-East 105F, New York, NY, USA
Phone: 212-305-9430; Fax: 212-305-4834; E-mail:

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