JCI table of contents: January 19, 2006

ity of these Tregs, preventing them from suppressing the ongoing immune response, and thus ensuring clearance of the infection. Once the fungus is cleared by the immune system, the source of the TLR2 ligand is no longer present, and the Tregs regain their suppressive capabilities. This explains how TLR2 can directly control Treg function and allows Tregs to behave differently before, during, and after infection. This control mechanism contributes to the balance between the mounting of an effective immune response and the development of autoimmunity.

TITLE: Toll-like receptor 2 controls expansion and function of regulatory T cells

Gosse J. Adema
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
Phone: 31-24-361-7600; Fax: 31-24-354-0339; E-mail: G.Adema@ncmls.ru.nl

View the PDF of this article at: https://www.the-jci.org/article.php?id=25439

Clues to rare immunodeficiency disorder identified

Patients who suffer from the rare, often fatal X-linked proliferative disease (XLP) have a severe deficiency of special immune cells called CD27+ (or memory) B cells, and are highly susceptible to infection with Epstein Barr Virus (EBV). XLP patients are characterized by hypogammaglobulinemia, infectious mononucleosis, and/or lymphoma. It was previously shown that XLP CD27+ cells also express a marker of nave B cells (IgM+) and it was unclear whether these IgM+CD27+ B cells in XLP patients could produce immunoglobulin (Ig) or function as normal memory B cells. New research by Stuart Tangye and colleagues at the Centenary Institute of Cancer Medicine and Cell Biology in Sydney, Australia demonstrates that these cells are indeed functional memory B cells. Their study, appearing online on January 19 in advance of print publication in the February 2006 issue o

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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