1. 病毒加重寄生生物疾病

有一种寄生生物会导致利什曼病(Leishmaniasis)，该病是一种皮肤溃疡性疾病，能通过[吸血的]白蛉(sandfly)传染到其他人或动物身上。当这种寄生生物被病毒感染后，它刺激宿主产生炎症性细胞因子，令人不解地地就是这些炎症性细胞因子能促进这种寄生生物的传播，从而造成更严重的疾病。

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.

2. 细胞因子，感染阻断物

病人被白念珠菌(Candida albicans)---为慢性皮肤黏膜念珠菌病(chronic mucocutaneous candidiasis disease, CMCD)的致病菌，能感染口腔黏膜和生殖道黏膜，皮肤和指甲---感染后，其体内编码白细胞介素-17受体A(interleukin-17 receptor A, IL-17RA)和IL-17F的基因经常会发生突变。金黄色葡萄球菌(Staphylococcus aureus)感染后可能也是如此。这表明这些细胞因子在抗感染方面发挥着关键性的作用。

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.

3. 病毒感染模式线虫

秀丽隐杆线虫(C. elegans)的第一次自然发生的病毒感染给研究人员提供一种遗传学上容易操作的模型，用来研究病毒-宿主相互作用，天然免疫(innate immunity)以及小RNA病毒防御的演化。

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.

4. 追踪IL-17

一种新的模式老鼠让研究人员可以追踪那些产生最近发现的细胞因子IL-17的细胞，甚至在细胞停止产生IL-17之后依然可以追踪，这样就可以清楚显示这些细胞发挥的有益性的和疾病性的作用。

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.

5. 调节性T细胞加快癌转移(metastasis)

人们过去认为调节性T细胞通过产生对癌耐受性的免疫细胞而有助于癌。如今，研究人员证实在乳癌中，调节性T细胞通过产生更多的NF-KB配体的受体或激活因子(Receptor or Activator of NF-KB Ligand, RANKL)而发挥着更积极性的作用，因为RANKL能促进癌转移。

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.

6. 嗜酸细胞支持产生抗体的细胞

嗜酸细胞(Eosinophil)，因加剧过敏性反应而广为人知，最近人们质疑它在抗寄生生物方面是否有用。而最新研究表明，在老鼠骨髓中，嗜酸细胞能帮助维持能产生抗体的浆细胞(plasma cell)的生存。

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.

7.攫取受体

除了结合抗原呈递细胞(antigen presenting cell)表面的CD80和CD86受体，削弱它们激活T细胞的能力之外，T辅助细胞表面的CTLA-4受体还能强行地攫取走这些受体，从而表明CTLA-4受体分子可能采取另一种机制抑制免疫性能。

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