Nature Studies – A mix bag of Immunology and Bacteria

Mucosal immunology: Infection induces friendly fire

http://www.nature.com/nature/journal/v490/n7418/full/490041a.html?WT.ec_id=NATURE-20121004#/affil-auth

03 October 2012

Our immune system usually ignores ‘friendly’ gut bacteria. But when infection with a pathogen damages the intestine’s mucosal lining, the resident microbes can invade the body, inducing immune responses directed at themselves.

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Pregnancy imprints regulatory memory that sustains anergy to fetal antigen – (Letter)

Cincinnati Children’s Hospital Medical Center, Division of Infectious Diseases, Cincinnati, Ohio

http://www.nature.com/nature/journal/v490/n7418/full/nature11462.html

Pregnancy is an intricately orchestrated process where immune effector cells with fetal specificity are selectively silenced. This requires the sustained expansion of immune-suppressive maternal FOXP3+ regulatory T cells (Treg cells), because even transient partial ablation triggers fetal-specific effector T-cell activation and pregnancy loss1, 2. In turn, many idiopathic pregnancy complications proposed to originate from disrupted fetal tolerance are associated with blunted maternal Treg expansion3, 4, 5. Importantly, however, the antigen specificity and cellular origin of maternal Treg cells that accumulate during gestation remain incompletely defined. Here we show that pregnancy selectively stimulates the accumulation of maternal FOXP3+ CD4 cells with fetal specificity using tetramer-based enrichment that allows the identification of rare endogenous T cells6. Interestingly, after delivery, fetal-specific Treg cells persist at elevated levels, maintain tolerance to pre-existing fetal antigen, and rapidly re-accumulate during subsequent pregnancy. The accelerated expansion of Treg cells during secondary pregnancy was driven almost exclusively by proliferation of fetal-specific FOXP3+ cells retained from prior pregnancy, whereas induced FOXP3 expression and proliferation of pre-existing FOXP3+ cells each contribute to Treg expansion during primary pregnancy. Furthermore, fetal resorption in secondary compared with primary pregnancy becomes more resilient to partial maternal FOXP3+ cell ablation. Thus, pregnancy imprints FOXP3+ CD4 cells that sustain protective regulatory memory to fetal antigen. We anticipate that these findings will spark further investigation on maternal regulatory T-cell specificity that unlocks new strategies for improving pregnancy outcomes and novel approaches for therapeutically exploiting Treg cell memory.
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This entry was posted in Autism, Immune System, Inflammation, Neurology, Physiology. Bookmark the permalink.

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