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![Commensal microbiota affects ischemic stroke outcome by regulating intestinal [gamma][delta] T cells : Nature Medicine : Nature Publishing Group | Immunopathology & Immunotherapy | Scoop.it](https://img.scoop.it/TRrxkpys-j5OIm8p8x6Ztjl72eJkfbmt4t8yenImKBVvK0kTmF0xjctABnaLJIm9)
Alterations in the gut microbiota affect stroke outcomes via modulation of T cells, suggesting a gut-brain axis linking commensal microbes with the CNS. 
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Here we report that proliferation of Treg cells after TCR stimulation is impaired in subjects with relapsing-remitting multiple sclerosis (RRMS) because of altered interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R)-signal ... Via Krishan Maggon
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Original article: http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3411.html NATURE MEDICINE | LETTER Regulatory T cell proliferative potential is impaired in human autoimmune diseaseFortunata Carbone,Veronica De Rosa,Pietro B Carrieri,Silvana Montella,Dario Bruzzese,Antonio Porcellini,Claudio Procaccini,Antonio La Cava& Giuseppe Matarese
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A new vaccine has been developed to act as a booster to Bacille Calmette Guerin (BCG), currently the only TB vaccine available. BCG was developed in the 1920s and has been used worldwide.
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Link to the Science Translational Medicine publication: http://stm.sciencemag.org/content/5/205/205ra134 Sci Transl Med 2 October 2013: Vol. 5, Issue 205, p. 205ra134 Sci. Transl. Med. DOI: 10.1126/scitranslmed.3006843A Human Type 5 Adenovirus–Based Tuberculosis Vaccine Induces Robust T Cell Responses in Humans Despite Preexisting Anti-Adenovirus ImmunityFiona Smaill1,2, Mangalakumari Jeyanathan1,3, Marek Smieja1,2, Maria Fe Medina1,3,Niroshan Thanthrige-Don1,3, Anna Zganiacz1,3, Cindy Yin1,3, Armando Heriazon1,3,Daniela Damjanovic1,3, Laura Puri1, Jemila Hamid1,4, Feng Xie4, Ronan Foley1,3,Jonathan Bramson1,2,3, Jack Gauldie1,2,3 and Zhou Xing1,2,3,*
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Who would dare to pit one fatal disease against another… inside the body of a six-year-old patient? The results will shatter all expectations.
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ROSS KAUFFMAN A seven-year-old girl has been 'cured' of leukaemia after a new therapy in which her T-cells — the immune system's killer cells — were bio-engineered to become 'guided missiles' to seek out and destroy the leukaemia, a new study shows. Read more: http://www.dailymail.co.uk/health/article-2246008/Girl-7-cured-leukaemia-scientists-reprogramme-immune-cells-destroy-cancer.html#ixzz2FFTBJNCy
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The Journal of Allergy and Clinical Immunology
High-throughput TCR sequencing of rare immune disorders has demonstrated that quantitative TCR diversity can appear normal despite qualitative changes in repertoire and strongly suggests that in human subjects RAG enzymatic function might be necessary for normal CDR3 junctional diversity.
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RT @RIRDF: NIH Scientists Identify a New Immunodeficiency Disease http://t.co/CP96Q4OVcI
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Link to the Nature Immunology Paper: http://www.nature.com/ni/journal/vaop/ncurrent/full/ni.2771.html ;
The study has identified a novel immunodeficiency disease called PASLI, its underlying genetic cause, and a promising, targeted treatment that is already FDA-approved for other purposes. The discovery of PASLI disease also contributes to our understanding of the immune system and highlights the role of PI3K-p110 delta and mTOR in immunity.
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Scientists have shown for the first time the effectiveness of a new technique that could allow the development of more-specific, cell-based immune therapies for cancer.
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Here you have the original publication in Nature Biotechnology:http://www.nature.com/nbt/journal/vaop/ncurrent/full/nbt.2459.html
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Commensal gut bacteria impact the host immune system and can influence disease processes in several organs, including the brain. However, it remains unclear whether the microbiota has an impact on the outcome of acute brain injury. Here we show that antibiotic-induced alterations in the intestinal flora reduce ischemic brain injury in mice, an effect transmissible by fecal transplants. Intestinal dysbiosis alters immune homeostasis in the small intestine, leading to an increase in regulatory T cells and a reduction in interleukin (IL)-17–positive γδ T cells through altered dendritic cell activity. Dysbiosis suppresses trafficking of effector T cells from the gut to the leptomeninges after stroke. Additionally, IL-10 and IL-17 are required for the neuroprotection afforded by intestinal dysbiosis. The findings reveal a previously unrecognized gut-brain axis and an impact of the intestinal flora and meningeal IL-17+ γδ T cells on ischemic injury.