JCI table of contents October 1, 2005

September 08, 2005



A number of studies suggest a protective action of the fatty acid DHA in cognitive decline and in Alzheimer disease (AD). However, the molecular mechanism is not understood. In a paper appearing online on September 8 in advance of print publication of the October 1 issue of the Journal of Clinical Investigation, Nicolas Bazan and colleagues from Louisiana State University identify a specific mechanism by which DHA is neuroprotective in AD.

The authors report that DHA can decrease levels of the pathogenic Abeta peptides that are associated with Alzheimer disease pathology in human brain cells. Meanwhile, the synthesis of neuroprotectin D1 (NPD1), an endogenous DHA-derived messenger, is upregulated. NPD1 inhibits apoptosis triggered by Abeta peptides. In a human AD donor brain, the authors show that DHA and NPD1 are reduced in vulnerable brain regions.

This data raises the possibility that NPD1 is a key regulator of cell survival, and might be manipulated for the development of novel therapeutic strategies for neurodegenerative diseases.

TITLE:A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease

(1) Nicolas Bazan
LSU Neuroscience Center of Excellence, New Orleans, LA USA
Phone: 504-599-0831; Fax: 504-568-5801; E-mail: nbazan@lsuhsc.edu

(2) Charles N. Serhan
Brigham and Women's Hospital, Boston, MA USA
Phone: 617-732-8822; Fax: 617-278-6957; E-mail: cnserhan@zeus.bwh.harvard.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=25420



Exposure to the chemical element beryllium can cause a disease characterized by circulating and proliferating CD4 positive immune T cells in the blood. Beryllium is used in nuclear reactors and as an aerospace structural material, putting workers at risk for chronic beryllium disease.

In a paper appearing online on September 8 in advance of print publication of the October 1 issue of the Journal of Clinical Investigation, Andrew Fontenot and colleagues from University of Colorado have investigated berylium-specific T cell responses in subjects exposed to beryllium in the workplace.

The authors show that beryllium-specific T cells with a central memory phenotype (CD45RA-/CCR7+) are responsible for the proliferative response, and T cells with an effector memory phenotype (CD45RA-/CCR7-) are primarily responsible for cytokine production.

These findings indicate that the proportion of memory T cells determines the function of antigen-specific CD4+ T cells. These findings have broad implications for all forms of organ-specific immune-mediated disease.

TITLE:Frequency of Beryllium-Specific, Central Memory CD4+ T Cells in Blood Determines Proliferative Response.

Andrew Fontenot
University of Colorado Health Sciences Center, Denver, CO USA
Phone: 303-315-1133; Fax: 303-315-7642; E-mail: andrew.fontenot@uchsc.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=24908



Infection with the pathogenic fungus Histoplasma capsulatum causes activation of the TNF-alpha protein, which is a determinant of protective immunity to both primary and secondary infection with the fungus. One of the major properties of TNF-alpha is to mediate apoptosis. In a paper appearing online on September 8 in advance of print publication of the October 1 issue of the Journal of Clinical Investigation, George Deepe and Holly Allen from the University of Cincinnati sought to determine if apoptosis contributed to the protective immune response.

The researchers find that apoptosis does occur during the course of infection and that the apoptotic cells are mostly T cells. Inhibiting apoptosis exacerbated disease, contrary to what one might expect for a pathogen that is heavily dependent on T cells for clearance. These findings provide new information regarding apoptosis and host regulation of immunity.

TITLE:Apoptosis Modulates Protective Immunity to the Pathogenic Fungus, Histoplasma capsulatum.

George Deepe
University of Cincinnati College of Medicine, Cincinnati, OH USA
Phone: 513-558-4704; Fax: 513-558-2089; E-mail: george.deepe@uc.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=25365



Human alpha1(IV)NC1 is a molecule derived from a part of collagen that can inhibit the formation of new blood vessels and tumor growth, but the mechanisms for this were not known. In a paper appearing online on September 8 in advance of print publication of the October 1 issue of the Journal of Clinical Investigation, Sudhakar Akulapalli and colleagues from Boys town national research hospital describe the complete signaling mechanism of the collagen-derived angiogenesis inhibitor alpha1(IV)NC1. The observations contribute to our understanding of the therapeutic potential of this molecule for the treatment of cancer.

TITLE:Human alpha1 type IV collagen NC1 domain exhibits distinct antiangiogenic activity mediated by alpha1beta1 integrin.

Sudhakar Akulapalli
Boys Town National Research Hospital, Omaha, NE USA
Phone: 402-498-6681; Fax: 402-498-6331; E-mail: akulapallis@boystown.org

View the PDF of this article at: https://www.the-jci.org/article.php?id=24813

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