EDITOR'S PICK: New drug targets for spinal cord injury?
Traumatic spinal cord injury causes permanent disability or loss of movement (paralysis) and sensation below the site of the injury. Currently, there are no treatments that can reverse the damage to the spinal cord, there are only approaches to prevent further damage and to help people return to an active lifestyle. However, Philip Popovich and colleagues, at the Ohio State University College of Medicine, Columbus, have studied the problem in mice and identified potential new therapeutic targets for minimizing injury and/or promoting repair after traumatic spinal cord injury
Traumatic injury to the spinal cord triggers a series of responses by the body that cause further damage to the spinal cord and additional loss of nerve cell function. One of these responses is activation of immune cells known as B cells. In the study, it was found that following traumatic spinal cord injury, mice lacking B cells showed improved recovery of movement when compared with normal mice. They also had a smaller area of damage in the spinal cord. Further analysis indicated that B cells worsened outcome in the mice by producing molecules known as antibodies and therefore the authors suggest that therapeutics that remove B cells or antibodies or that inhibit B cell responses might be of benefit to individuals who experience traumatic spinal cord injury.
In an accompanying commentary, Gregory Dekaban and Sakina Thawer, at the Robarts Research Institute, Canada, concur that such approaches should be considered, although they caution that studies confirming the importance of B cells in causing damage following spinal cord injury in humans need to be performed.
TITLE: B cells produce pathogenic antibodies and impair recovery after spinal cord injury in mice
AUTHOR CONTACT:
Phillip G. Popovich
The Ohio State University College of Medicine, Columbus, Ohio, USA.
Phone: (614) 688-8576; Fax: (614) 688-5463; E-mail: phillip.popovich@osumc.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=39780
ACCOMPANYING COMMENTARY
TITLE: Pathogenic antibodies are active participants in spinal cord injury
AUTHOR CONTACT:
Gregory A. Dekaban
Robarts Research Institute, London, Ontario, Canada.
Phone: (519) 663-5777 Ext. 24241; Fax: (519) 391-5789; E-mail: dekaban@robarts.ca.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40839
EDITOR'S PICK: Distinguishing breast cancer–causing mutations from those that are harmless
Women with mutations in either their BRCA1 or BRCA2 genes have a dramatically increased risk of developing breast or ovarian cancer. Identifying such women provides them with an opportunity to take preventive measures such as surgery to remove their breasts. One caveat to identifying such women by simply sequencing their BRCA1 and BRCA2 genes and detecting mutations is that not all mutations are harmful. However, Shyam Sharan and colleagues, at the National Cancer Institute at Frederick, have now developed an assay to distinguish harmful BRCA1 mutations from those that are not. As discussed by the authors and, in an accompanying commentary, Roger Greenberg, this assay has immense clinical potential to identify those patients that might benefit from treatments to prevent breast cancer.
TITLE: Expression of human BRCA1 variants in mouse ES cells allows functional analysis of BRCA1 mutations
AUTHOR CONTACT:
Shyam K. Sharan
National Cancer Institute at Frederick, Frederick, Maryland, USA.
Phone: (301) 846-5140; Fax: (301) 846-7017; E-mail: sharans@mail.nih.gov.
View the PDF of this article at: https://www.the-jci.org/article.php?id=39836
ACCOMPANYING COMMENTARY
TITLE: Breast cancer gene variants: separating the harmful from the harmless
AUTHOR CONTACT:
Roger A. Greenberg
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 746-2738; Fax: (215) 573-2486; E-mail: rogergr@mail.med.upenn.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40577
NEPHROLOGY: Understanding a cause of a major complication of chronic kidney disease
TITLE: The peptidyl-prolyl isomerase Pin1 determines parathyroid hormone mRNA levels and stability in rat models of secondary hyperparathyroidism
AUTHOR CONTACT:
Tally Naveh-Many
Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Phone: 972-2-6776789; Fax: 972-2-6421234; E-mail: tally@huji.ac.il.
View the PDF of this article at: https://www.the-jci.org/article.php?id=39522
ACCOMPANYING COMMENTARY
TITLE: Pin1 regulates parathyroid hormone mRNA stability
AUTHOR CONTACT:
Rajiv Kumar
Mayo Clinic and Foundation, Rochester, Minnesota, USA.
Phone: (507) 284-0020; Fax: (507) 538-9536; E-mail: rkumar@mayo.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40784
IMMUNOLOGY: The thymus stops the immune system ageing prematurely
TITLE: Evidence of premature immune aging in patients thymectomized during early childhood
AUTHOR CONTACT:
Victor Appay
INSERM U945, Hôpital Pitié-Salpêtrière, Paris, France.
Phone: 33-1-40-77-81-83; Fax: 33-1-42-17-74-90; E-mail: victor.appay@upmc.fr.
View the PDF of this article at: https://www.the-jci.org/article.php?id=39269
ACCOMPANYING COMMENTARY
TITLE: Reduced thymus activity and infection prematurely age the immune system
AUTHOR CONTACT:
Steven G. Deeks
University of California at San Francisco, San Francisco, California, USA.
Phone: (415) 476-4082 ext. 404; Fax: (415) 476-6953; Email: sdeeks@php.ucsf.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40855
PULMONARY: Immune cells known as Tregs promote recovery from acute lung injury
TITLE: CD4+CD25+Foxp3+ Tregs resolve experimental lung injury in mice and are present in humans with acute lung injury
AUTHOR CONTACT:
Landon S. King
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Phone: (443) 287-3343; Fax: (443) 287-3349; E-mail: lsking@jhmi.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=36498
ACCOMPANYING COMMENTARY
TITLE: Resolving lung injury: a new role for Tregs in controlling the innate immune response
AUTHOR CONTACT:
Steve N. Georas
University of Rochester Medical Center, Rochester, New York, USA.
Phone: (585) 275-4861; Fax: (585) 275-1171; E-mail: Steve_Georas@urmc.rochester.edu.
Anthony Pietropaoli
University of Rochester Medical Center, Rochester, New York, USA.
Phone: (585) 275-4861; Fax: (585) 275-1171; E-mail: Anthony_Pietropaoli@urmc.rochester.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40880
BONE BIOLOGY: Controlling how many bone destroying cells are present in inflammatory situations
TITLE: NF-kappa-B p100 limits TNF-induced bone resorption in mice by a TRAF3-dependent mechanism
AUTHOR CONTACT:
Brendan F. Boyce
University of Rochester Medical Center, Rochester, New York, USA.
Phone: (585) 275-5837; Fax: (585) 273-3637; E-mail: Brendan_Boyce@urmc.rochester.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=38716
ACCOMPANYING COMMENTARY
TITLE: NF-kappa-B2 (p100) limits TNF-alpha–induced osteoclastogenesis
AUTHOR CONTACT:
Sakae Tanaka
The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Phone: 81-3-3815-5411 ext. 33376; Fax: 81-3-3818-4082; E-mail: tanakas-ort@h.u-tokyo.ac.jp.
View the PDF of this article at: https://www.the-jci.org/article.php?id=40629
Journal
Journal of Clinical Investigation