JCI table of contents: April 22, 2008

In the study, the T cell loss caused by the Edmonton protocol was shown to be associated with the production of soluble factors that stimulate T cell proliferation as well as an increase in the number of T cells that recognize a protein (GAD65) expressed by islet cells. In two transplant recipients studied, two of the drugs in the Edmonton protocol (FK506 and rapamycin) were replaced with an alternative (micophenolate mofetil). No increase in the number of T cells that recognize GAD65 was observed in these individuals, leading the authors to suggest that drug regimens that do not promote the expansion of T cells might improve the outcome of islet cell transplantation. The importance of these observations for the ongoing development of new protocols for ensuring islet cell transplant survival is discussed in an accompanying commentary by Tom Van Belle and Matthias von Herrath, at the La Jolla Institute for Allergy and Immunology.

TITLE: Islet transplantation in patients with autoimmune diabetes induces homeostatic cytokines that expand autoreactive memory T cells

AUTHOR CONTACT:
Ezio Bonifacio
Dresden University of Technology, Dresden, Germany.
Phone: 49-0-351-463-40092; Fax: 49-0-351-463-40090; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=35197

ACCOMPANYING COMMENTARY
TITLE: Immunosuppression in islet transplantation

AUTHOR CONTACT:
Matthias von Herrath
La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
Phone: (858) 752-6817; Fax: (858) 752-6993; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=35639

NEUROBIOLOGY: One protein, opposite effects on a characteristic of some neurodegenerative disorders

One of the characteristics of the brain of people with Alzheimer disease (AD) is the presence of tangles, insoluble twisted fibers that build up inside the nerve cells of the brain resulting in malfunctions in communication between nerves and later in their death. As these tangles are due to abnormal aggregation of the tau protein, AD is classified as a tauopathy. Other tauopathies include the neurodegenerative disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Although the tau protein in individuals with AD is not mutated, mice carrying the mutated forms of tau found in individuals with FTDP-17 are often used as mouse models of AD. However, Kun Ping Lu and colleagues, at Harvard Medical School, Boston, have now determined that nonmutated tau protein and the most frequent form of mutant tau in individuals with FTDP-17 (P301L tau) are regulated differently by the protein Pin1, meaning that mice carrying mutated forms of tau are not likely to model AD very faithfully.