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[The Scientist: June 6, 2011 by Edyta Zielinska]

1. 從外面感染

人們長期認為的細菌感染模型遭受挑戰(zhàn)，因為研究人員證實毒性因子(virulence factor)能夠從致病菌的表面，而不是從它的細胞質(zhì)(cytosol)，轉(zhuǎn)移到宿主細胞，從而就為疫苗和治療方法設(shè)計提供新的靶標。

K. Akopyan et al., “Translocation of surface-localized effectors in type III secretion,”PNAS,108:1639-44, 2011. Evaluated by Arto Pulliainen and Christoph Dehio, Biozentrum, Univ of Basel, Switzerland; Fabio Bagnoli and Rino Rappuoli, Novartis Vaccines and Diagnostics Srl, Italy; Raphael Valdivia, Duke Univ Med Cntr; Olivia Steele-Mortimer, Rocky Mountain Labs, NIAID; Mélanie Hamon and Pascale Cossart, Inst Pasteur, France; Peter Hume and Vassilis Koronakis, Univ of Cambridge, UK.

嗜中性粒細胞經(jīng)內(nèi)皮遷移(neutrophil transendothelial migration)，化學運動性(chemokinesis)和吞噬細菌(圖片來自Greg Luerman)

2. 巨噬細胞激發(fā)癌癥免疫性(cancer immunity)

吞噬已死的癌細胞的巨噬細胞可能要比樹突細胞(dendritic cell)在激活殺死腫瘤的T細胞方面發(fā)揮著更大的作用，在激活對抗癌癥的免疫方面，這一結(jié)果或許有助于疫苗和免疫治療設(shè)計。

K. Asano et al., “CD169-positive macrophages dominate antitumor immunity by crosspresenting dead cell-associated antigens,” Immunity, 34:85-95, 2011. Evaluated by Xiaojing Ma, Weill Med Col of Cornell Univ; Lieping Chen, Yale Univ Sch of Med; Peter Van Endert, Inst National de la Sante et de la Recherche Medicale, France; Peter Murray, St. Jude Children’s Res Hosp; Christian Engwerda, Queensland Inst of Med Res, Australia; David Kranz, Univ of Illinois at Urbana-Champaign.

3. 藥物影響細菌進化

肺炎鏈球菌(Streptococcus pneumonia)要比研究人員想象中更快地適應(yīng)臨床干預(clinical intervention)，從而表明臨床干預在這種細菌的多耐藥菌株進化上的影響。

N.J. Croucher et al., “Rapid pneumococcal evolution in response to clinical interventions,” Science, 331:430-34, 2011. Evaluated by Scott Chancey and David Stephens, Emory Univ; Mark Enright, Biocontrol Limited., UK.

4. 重新激活抑制性T細胞(suppressive T cell)

免疫抑制性的調(diào)節(jié)性T細胞(T-regulatory cell)能夠打開開關(guān)，使得免疫性得以激活，在適應(yīng)性免疫反應(yīng)中發(fā)揮著關(guān)鍵性的作用。然而，癌細胞能夠破壞這個過程，以便在免疫抑制性條件下茁長成長。

M.D. Sharma et al., “Reprogrammed foxp3(+) regulatory T cells provide essential help to support cross-presentation and CD8(+) T cell priming in naive mice,” Immunity,  33:942-54, 2010. Evaluated by Mark Doherty, Statens Serum Inst, Denmark; Ru Zhou and Rachel R Caspi, National Eye Institute, NIH; Thomas Huenig, Univ of Wurzberg, Germany.

5. 晶體與免疫細胞

明礬佐劑(Alum)，一種添加到疫苗中的一般性免疫促進劑，是一個晶體，它的作用模式長期以來都是一個謎?，F(xiàn)在，研究人員證實它通過以下方式發(fā)揮作用，抓住樹突細胞(dendritic cell)的脂質(zhì)，從而促進疫苗抗原的攝取以及隨后樹突細胞調(diào)節(jié)的免疫激活。

T. L. Flach et al., “Alum interaction with dendritic cell membrane lipids is essential for its adjuvanticity,” Nat Med, 17:479-87, 2011. Evaluated by Mark Doherty, Statens Serum Inst, Denmark;David Underhill, Cedars-Sinai Med Cent.

6. 發(fā)現(xiàn)新病毒和疾病

研究人員在171名中國病人樣品中發(fā)現(xiàn)了一種威脅人類生命的新病毒，稱作嚴重發(fā)熱性血小板減少綜合癥布尼亞病毒[severe fever with thrombocytopenia syndrome (SFTS) bunyavirus]。該病毒是以它導致的嚴重性發(fā)熱伴隨著血小板減少的綜合癥命名的，該疾病的特征是低的血小板數(shù)量和胃腸道癥狀。

X.J. Yu et al., “Fever with thrombocytopenia associated with a novel bunyavirus in China,” N Engl J Med, 364:1523-32, 2011. Evaluated by Charles Chiu, UCSF; David Wang, Washington Univ in St. Louis.

7. 證實HPV疫苗有效

對10萬多名澳大利亞病人的一份研究證實了一種人乳頭狀瘤病毒(human papillomavirus, HPV)疫苗能有效地抗擊產(chǎn)生生殖器疣(genital-wart)和誘發(fā)癌癥的病毒毒株。在ZF資助的疫苗接種項目開始之后，在女性身上觀察的生殖器疣病例下降了將近60%。

B. Donovan et al., “Quadrivalent human papillomavirus vaccination and trends in genital warts in Australia: analysis of national sentinel surveillance data,” Lancet Infect Dis, 11:39-44, 2011. Evaluated by  Christian Wejse and Lars Ostergaard Aarhus Univ Hosp, Denmark.