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| 1 | Identification of four novel DC-SIGN ligands on Mycobacterium bovis BCG显示文摘Dendritic-cell-specific intercellular adhesion molecule-3-grabbing non-integrin(DC-SIGN;CD209)has an important role in mediating adherence of Mycobacteria species,including M.tuberculosis and M.bovis BCG to human dendritic cells and macrophages,in which these bacteria can survive intracellularly.DC-SIGN is a C-type lectin,and interactions with mycobacterial cells are believed to occur via mannosylated structures on the mycobacterial surface.Recent studies suggest more varied modes of binding to multiple mycobacterial ligands.Here we identify,by affinity chromatography and mass-spectrometry,four novel ligands of M.bovis BCG that bind to DC-SIGN.The novel ligands are chaperone protein DnaK,60 kDa chaperonin-1(Cpn60.1),glyceraldehyde-3 phosphate dehydrogenase(GAPDH)and lipoprotein lprG.Other published work strongly suggests that these are on the cell surface.Of these ligands,lprG appears to bind DC-SIGN via typical proteinglycan interactions,but DnaK and Cpn60.1 binding do not show evidence of carbohydrate-dependent interactions.LprG was also identified as a ligand for DC-SIGNR(L-SIGN;CD299)and the M.tuberculosis orthologue of lprG has been found previously to interact with human toll-like receptor 2.Collectively,these findings offer new targets for combating mycobacterial adhesion and within-host survival,and reinforce the role of DCSIGN as an important host ligand in mycobacterial infection. | Maria V.Carroll Robert B.Sim Fabiana Bigi Anne Jäkel Robin Antrobus Daniel A.Mitchell | 2010 | Protein & Cell2010，1，9： | 7 |
| 2 | Tinker,tailor,soldier,cell:the role of C-type lectins in the defense and promotion of disease显示文摘C-type lectins(CTLs)represent a large family of soluble and membrane-bound proteins which bind calcium dependently via carbohydrate recognition domains(CRDs)to glycan residues presented on the surface of a variety of pathogens.The deconvolution of a cell’s glycan code by CTLs underpins several important physiological processes in mammals such as pathogen neutralization and opsonization,leukocyte trafficking,and the inflammatory response.However,as our knowledge of CTLs has developed it has become apparent that the role of this innate immune family of proteins can be double-edged,where some pathogens have developed approaches to subvert and exploit CTL interactions to promote infection and sustain the pathological state.Equally,CTL interactions with host glycoproteins can contribute to inflammatory diseases such as arthritis and cancer whereby,in certain contexts,they exacerbate inflammation and drive malignant progression.This review discusses the‘dual agent’roles of some of the major mammalian CTLs in both resolving and promoting infection,inflammation and inflammatory disease and highlights opportunities and emerging approaches for their therapeutic modulation. | James N.Arnold Daniel A.Mitchell | 2023 | Protein & Cell2023，14，1： | 1 |
| 3 | 把律师和委托人的利益结合起来显示文摘众所周知,律师与委托人之间存在潜在冲突。如果一位律师的收入只与他所付出的时间相关而与案件的结果无关,那么律师可能会希望将案件提起诉讼,即便是提起诉讼并不符合委托人的最佳利益,律师也可能会在该案件上耗费比委托人所期望的更多的工作时间,也可能在和解对于委托人更为有利的时候反对和解。反之,如果律师是根据传统的风险代理收费方式来获得报酬——根据这种收费方式,他只能获得判决所得或者和解所得的一部分,却必须承担所有的诉讼成本——那么,律师可能没有什么动力将案件提起诉讼,或即便提起诉讼的话也可能会花很少的时间在该案件上,也可能当提起诉讼对于委托人来说更为有利的时候却鼓励他们进行和解。在这篇论文中,我们提出一种支付律师报酬的方式,这种方式能够克服律师和委托人之间的利益冲突。我们的方式是传统风险代理收费方式的一种变体,但是相比于传统风险代理收费方式来说,我们将会使律师仅仅承担诉讼成本的一部分。同样,律师在判决所得或者和解所得中也只能获得一部分回报。我们证明,当律师所承担的成本份额等于他能够从判决中所得或者和解中所获得的回报份额,那么他就有动力完全按照一个有见地(knowledgeable)的委托人对他的期望来开展工作,比如在是否将案件提起诉讼、在案件上花费多少时间以及是否对案件进行和解等方面。根据我们的改良风险代理收费方式,第三方将偿付律师费用的一部分,作为回报,律师将事先支付给该第三方一笔费用。通过这种方式,即便案件败诉了,委托人也不用像传统风险代理收费方式那样承担任何费用。 | Daniel L.Rubinfeld 吴洪淇(译) | 2008 | 私法2008，，1： | 0 |
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