Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. Signal., 1 May 2012
Vol. 5, Issue 222, p. ec126
[DOI: 10.1126/scisignal.2003169]

EDITORS' CHOICE

Immunology Gut Reaction

Kristen Mueller

Science, AAAS, Washington, DC 20005, USA

The gut needs to keep its trillions of microbial inhabitants contained. The immune system has evolved a multifaceted approach to this problem, which includes the production of large quantities of immunoglobulin A (IgA) in the intestinal mucosa. In a process that is not well understood, plasma cells that produce IgA specific for the gut microflora are selected in Peyer’s patches in the gut. Kawamoto et al. used genetically manipulated mice to show that the inhibitory co-receptor programmed cell death–1 (PD-1) is required for the proper selection of IgA-secreting cells in the gut. The effect of PD-1 deletion, however, was not intrinsic to the B cells that produce IgA. Instead, the absence of PD-1 affected the differentiation of T follicular helper cells, which provide important signals to B cells that help guide them as they develop the capacity to produce microflora-specific IgA. Mice deficient in PD-1 exhibited alterations in the composition in their microflora, which suggests that defective selection of IgA can perturb the careful balance that exists between the immune system and resident bacteria.

S. Kawamoto, T. H. Tran, M. Maruya, K. Suzuki, Y. Doi, Y. Tsutsui, L. M. Kato, S. Fagarasan, The inhibitory receptor PD-1 regulates IgA selection and bacterial composition in the gut. Science 336, 485–489 (2012). [Abstract] [Full Text]

Citation: K. Mueller, Gut Reaction. Sci. Signal. 5, ec126 (2012).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882