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JCI table of contents -- July 26, 2007

to involve toll-like receptor 4. Conversely, a reduction in the number of host microorganisms by the use of antibiotics reduced the beneficial effects of TBI on tumor regression in these animals. In summary, the results of the study demonstrate that the disruption of the host/microorganism balance by TBI and the resulting transient bacterial infection is a key mechanism driving the increased reactivity of tumor-specific CD8+ T cells and subsequent tumor regression in mice.

TITLE: Microbial translocation augments the function of adoptively transferred self/tumor-specific CD8+ T cells via TLR4 signaling

AUTHOR CONTACT:

Nicholas P. Restifo or Chrystal M. Paulos

National Cancer Institute, Bethesda, Maryland, USA.

Phone : (301) 496-4904; Fax : (310) 496-0011; E-mail: restifo@nih.gov or paulosc@mail.nih.gov

View the PDF of this article at: https://www.the-jci.org/article.php?id=32205


PHYSIOLOGY

A step forward in our understanding of tissue damage after spinal cord injury

Acute spinal cord injury can damage spinal cord tissue and result in loss of functions such as mobility or feeling. In a study appearing online on July 26 in advance of publication in the August print issue of the Journal of Clinical Investigation, J. Marc Simard and colleagues from the University of Maryland at Baltimore show that calcium-activated cation channels in capillaries surrounding spinal cord tissue are critical to the process that causes spinal cord tissue loss after acute cord injury, and as such are a potential target in the therapy of spinal cord injuries.

The authors showed that spinal cord injury in otherwise healthy rats caused a lesion in spinal cord tissue that progressively expanded in size and was accompanied by a fragm
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Contact: Brooke Grindlinger
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
26-Jul-2007


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