Ulcerative colitisWIKIMEDIA COMMONS
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
2. TRIMming retroviral infections
TRIM5, a ubiquitin ligase that helps thwart retroviral infections, works by promoting innate immune signaling and acting as a pattern recognition receptor that binds the retrovirus capsid lattice, adding to a growing list of TRIMs that regulate innate immune responses.
T. Pertel et...
Researchers engineered a GFP expressing mouse that can help researcher track the strength of T-cell receptor binding, creating a tool that may reveal how T-cells mature and the strength of signal required for the activation of various T-cell subtypes.
A.E. Moran et al., "T cell receptor signal strength in Treg and iNKT cell development demonstrated by a novel fluorescent reporter mouse,"J Exp Med, 208:1279-89, 2011. Evaluated by Astar Winoto, Univ of California, Berkeley; Ellen Robey, Univ of California, Berkeley; Scott Lieberman and Laurence Turka, Beth Israel Deaconess Med Cen. Free F1000 evaluation
4. Linking genes and bacteria in colitis
Mice that lack a gene for a key component of the immune system are more susceptible to colitis, and develop a gut-microbe enriched in one type bacteria. Furthermore, when mice that had a functional copy of the innate component are housed with knockout mice lacking the gene, both groups are susceptible to colitis, suggesting that gut microbial composition of the knockout mice spreads to the wild-type, and that both genes and microbes are involved in this autoimmune disease.
E. Elinav et al., "NLRP6 inflammasome regulates colonic microbial ecology and risk for colitis," Cell, 145:745-57, 2011. Evaluated by Lisa Maier and Wolf-Dietrich Hardt, Swiss Federal Inst of Tech (ETH), Switzerland; Peter Murray, St. Jude Children's Res Hosp; Kim Newton and Vishva Dixit, Genentech. Free F1000 evaluation
5. Regulation of autoimmune factor revealed
IL-2 is a cytokine essential to many kinds of immune activation, as well as suppressing autoimmune-disease-associated cytokine IL-17. Now researchers have shown that IL-2 suppresses IL-17 via STAT5, a transcription factor that binds and blocks regions of the IL-17 gene that are normally bound and activated by STAT3.
X.P. Yang et al., "Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5," Nat Immunol, 12:247-54, 2011. Evaluated by Allen Ho, Abhishek V. Garg and Sarah Gaffen, Univ of Pittsburgh; Patrick Walsh and Padraic Fallon, Trinity Col Dublin, Ireland; Wuzhou Wan and Philip Murphy, NIAID. Free F1000 evaluation
A human trial of anti-cancer combination therapy reveals that an antibody designed to activate CD40 receptor, which reactivates suppressed anti-cancer immunity, functions by turning on macrophages rather than T cells, resulting in cancer regression in some patients.
G.L. Beatty et al.,"CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans," Science, 331:1612-16, 2011. Evaluated by Rienk Offringa, German Cancer Res Cen (DKFZ); Albert Deisseroth, Sidney Kimmel Cancer Center. Free F1000 evaluation
Researchers find a new link between inflammation and apoptosis via the Bcl-2 family member BID. A known player in apoptosis, the BID signaling molecule was also shown to play an important role in conveying inflammatory signals.
G. Yeretssian et al., "Non-apoptotic role of BID in inflammation and innate immunity," Nature, 474:96-99, 2011. Evaluated by Brigitte Huber, Tufts Univ Sch of Med. Free F1000 evaluation
The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 in immunology and related areas, as calculated on June 16, 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 http://f1000.com.
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