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000170400 1001_ $$0P:(DE-He78)3ac0bc7cf0e8ab1e1bc05c7889bfa3df$$aJarahian, Mostafa$$b0$$eFirst author
000170400 245__ $$aActivating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein.
000170400 260__ $$aSydney$$bKarger$$c2022
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000170400 500__ $$a#EA:G401# / 2022;14(2):135-147
000170400 520__ $$aExpression of the extensively glycosylated Ebolavirus glycoprotein (EBOV-GP) induces physical alterations of surface molecules and plays a crucial role in viral pathogenicity. Here we investigate the interactions of EBOV-GP with host surface molecules using purified EBOV-GP, EBOV-GP-transfected cell lines, and EBOV-GP-pseudotyped lentiviral particles. Subsequently, we wanted to examine which receptors are involved in this recognition by binding studies to cells transfected with the EBOV-GP as well as to recombinant soluble EBOV-GP. As the viral components can also bind to inhibitory receptors of immune cells (e.g., Siglecs, TIM-1), they can even suppress the activity of immune effector cells. Our data show that natural killer (NK) cell receptors NKp44 and NKp46, selectins (CD62E/P/L), the host factors DC-SIGNR/DC-SIGN, and inhibitory Siglecs function as receptors for EBOV-GP. Our results show also moderate to strong avidity of homing receptors (P-, L-, and E-selectin) and DC-SIGNR/DC-SIGN to purified EBOV-GP, to cells transfected with EBOV-GP, as well as to the envelope of a pseudotyped lentiviral vector carrying the EBOV-GP. The concomitant activation and inhibition of the immune system exemplifies the evolutionary antagonism between the immune system and pathogens. Altogether these interactions with activating and inhibitory receptors result in a reduced NK cell-mediated lysis of EBOV-GP-expressing cells. Modulation of these interactions may provide new strategies for treating infections caused by this virus.
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000170400 650_7 $$2Other$$aEbolavirus glycoprotein
000170400 650_7 $$2Other$$aHPV
000170400 650_7 $$2Other$$aNatural cytotoxicity receptors
000170400 650_7 $$2Other$$aSelectins
000170400 650_7 $$2Other$$aSiglecs
000170400 7001_ $$0P:(DE-He78)ca88d821f0916f86f2e3b130f9cbe1eb$$aMarstaller, Katharina$$b1
000170400 7001_ $$0P:(DE-He78)e33dd4f0f85f24d38c389c3e9fa46854$$aBanna, Nadine$$b2$$udkfz
000170400 7001_ $$aAhani, Roshanak$$b3
000170400 7001_ $$aEtemadzadeh, Mohammad Hossein$$b4
000170400 7001_ $$aBoller, Lea K$$b5
000170400 7001_ $$aAzadmanesh, Kayhan$$b6
000170400 7001_ $$0P:(DE-He78)a30064f6b2d9ab959d35315d7668c091$$aCid-Arregui, Angel$$b7$$udkfz
000170400 7001_ $$aKhezri, Abdolrahman$$b8
000170400 7001_ $$0P:(DE-He78)7e60033e3eaaebb9ba30c905ade4a676$$aBerger, Martin R$$b9$$udkfz
000170400 7001_ $$0P:(DE-He78)b2290261145f21c46f2d42783c69d104$$aMomburg, Frank$$b10$$udkfz
000170400 7001_ $$aWatzl, Carsten$$b11
000170400 773__ $$0PERI:(DE-600)2455818-7$$a10.1159/000517628$$gp. 1 - 13$$n2$$p135-147$$tJournal of innate immunity$$v14$$x1662-8128$$y2022
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