IMAGE: WIKIMEDIA1. Virus amps up parasite disease

When the parasite that causes Leishmaniasis, a skin-ulcer disease transmitted by sandflies, is infected with a virus, it causes a more severe disease than when it is not infected, by triggering inflammatory cytokines in the host that paradoxically promote parasite's spread.

A. Ives et al., "Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis," Science, 331:775-78, 2011. Evaluated by Jan Rehwinkel and Caetano Reis e Sousa, Cancer Research UK; Breck Duerkop and Lora Hooper, U of Texas Southwestern Med Ctr; Heidi Snider and Abhay Satoskar, Ohio State Univ; Barbara Papadopoulou, Laval Univ, Canada; Jean-Luc Imler, Univ de Strasbourg, France; Christian Engwerda, Queensland Inst of Med Res, Australia. Free F1000 Evaluation

2. Cytokines, infection blockers Patients infected by Candida albicans -- the causative agent of chronic mucocutaneous candidiasis disease (CMCD), an infection of the oral and genital mucosae, skin, and nails -- and...

A. Puel et al., "Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity," Science, 332:65-8, 2011. Evaluated by Dan Conrad, Virginia Commonwealth Univ; Jay Kolls, LSU Health Sciences Cen; Klaus Ley, La Jolla Inst for Allergy & Immunology; Sarah Gaffen, Univ Pitt; Joshua Milner, National Inst of Allergy and Infectious Diseases. Free F1000 Evaluation

3. Virus infects model worm

The first naturally occurring virus infection in C. elegans provides researchers with a genetically tractable model for studying virus-host interactions, innate immunity and the evolution of small RNA viral defenses.

M.A. Felix et al., "Natural and experimental infection of caenorhabditis nematodes by novel viruses related to nodaviruses," PLoS Biol, 9:e1000586, 2011. Evaluated by Benjamin Podbilewicz, Technion- Israel Inst of Tech, Israel; Jean-Luc Imler, Univ de Strasbourg, France; Morris F Maduro, Univ California Riverside. Free F1000 Evaluation

4. Tracking IL-17

A new mouse model lets researchers follow the cells that produce the recently discovered IL-17 cytokine, even after the cells stop producing it, shedding light on the pathological and helpful roles these cells play.

K. Hirota et al., "Fate mapping of IL-17-producing T cells in inflammatory responses," Nat Immunol, 12:255-63, 2011. Evaluated by Alain Dessein, INSERM, France; Reiko Horai and Rachel R Caspi, National Eye Inst, NIH; Tzong-Shyuan Tai and I-Cheng Ho, Brigham & Women's Hospital; Oberdan Leo and Muriel Moser, University of Brussels, Belgium; Linda Bradley, Burnham Institute for Medical Research; Dan Conrad, Virginia Commonwealth University. Free F1000 Evaluation

5. T-regs accelerate metastasis

T-regulatory cells were thought to contribute to cancer by making immune cells tolerant to it. Now researchers show that T-regs take a more active role by producing RANKL in breast cancer, a factor that drives metastasis.

W. Tan et al., "Tumour-infiltrating regulatory T cells stimulate mammary cancer metastasis through RANKL-RANK signaling," Nature 470:548-53, 2011. Evaluated by Albert Deisseroth, Sidney Kimmel Cancer Ctr; David Richards and Markus Feuerer, German Cancer Res Ctr (DKFZ);| Mark Boothby, Vanderbilt Univ Sch of Med; Lynn Heltemes-Harris and Michael Farrar, U of Minnesota. Free F1000 Evaluation

6. Support for antibody-producing cells

Eosinophils, best known for exacerbating allergies and recently questioned for their usefulness in fighting parasites, were shown to help maintain the survival of antibody-producing plasma cells in the bone marrow of mice.

V.T. Chu et al., "Eosinophils are required for the maintenance of plasma cells in the bone marrow," Nat Immunol, 12:151-19, 2011. Evaluated by Dhaya Seshasayee and Flavius Martin, Genentech; Helene Rosenberg, LAD/NIAID/NIH; Naomi Harwood and Facundo Batista, London Res Inst, Cancer Res UK; Marion Espeli and Ken Smith, U of Cambridge, UK; Shinsuke Taki, Shinshu U Grad Sch of Med, Japan. Free F1000 Evaluation

7. Receptor-snatching

In addition to binding the CD80 and CD86 receptors on the surface of antigen presenting cells, impairing their ability to activate T cells, the CTLA-4 receptor on T helper cells can physically snatch away the receptors, demonstrating another mechanism by which this molecule may suppress immunity.

O.S. Qureshi et al., "Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4," Science, 332:600-3, 2011. Evaluated by Lieping Chen, Yale Univ Sch of Med; Amnon Altman, La Jolla Inst for Allergy and Immunology; Oberdan Leo and Muriel Moser, U of Brussels, Belgium. Free F1000 Evaluation

The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 Immunology, as calculated on May 12, 2011. Faculty Members evaluate and rate the most important papers in their field. To see the latest rankings, search the database, and read daily evaluations, visit

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