Home > Publications database > Activating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein. > print |
001 | 170400 | ||
005 | 20240229133712.0 | ||
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100 | 1 | _ | |a Jarahian, Mostafa |0 P:(DE-He78)3ac0bc7cf0e8ab1e1bc05c7889bfa3df |b 0 |e First author |
245 | _ | _ | |a Activating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein. |
260 | _ | _ | |a Sydney |c 2022 |b Karger |
336 | 7 | _ | |a article |2 DRIVER |
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500 | _ | _ | |a #EA:G401# / 2022;14(2):135-147 |
520 | _ | _ | |a Expression 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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650 | _ | 7 | |a Ebolavirus glycoprotein |2 Other |
650 | _ | 7 | |a HPV |2 Other |
650 | _ | 7 | |a Natural cytotoxicity receptors |2 Other |
650 | _ | 7 | |a Selectins |2 Other |
650 | _ | 7 | |a Siglecs |2 Other |
700 | 1 | _ | |a Marstaller, Katharina |0 P:(DE-He78)ca88d821f0916f86f2e3b130f9cbe1eb |b 1 |
700 | 1 | _ | |a Banna, Nadine |0 P:(DE-He78)e33dd4f0f85f24d38c389c3e9fa46854 |b 2 |u dkfz |
700 | 1 | _ | |a Ahani, Roshanak |b 3 |
700 | 1 | _ | |a Etemadzadeh, Mohammad Hossein |b 4 |
700 | 1 | _ | |a Boller, Lea K |b 5 |
700 | 1 | _ | |a Azadmanesh, Kayhan |b 6 |
700 | 1 | _ | |a Cid-Arregui, Angel |0 P:(DE-He78)a30064f6b2d9ab959d35315d7668c091 |b 7 |u dkfz |
700 | 1 | _ | |a Khezri, Abdolrahman |b 8 |
700 | 1 | _ | |a Berger, Martin R |0 P:(DE-He78)7e60033e3eaaebb9ba30c905ade4a676 |b 9 |u dkfz |
700 | 1 | _ | |a Momburg, Frank |0 P:(DE-He78)b2290261145f21c46f2d42783c69d104 |b 10 |u dkfz |
700 | 1 | _ | |a Watzl, Carsten |b 11 |
773 | _ | _ | |a 10.1159/000517628 |g p. 1 - 13 |0 PERI:(DE-600)2455818-7 |n 2 |p 135-147 |t Journal of innate immunity |v 14 |y 2022 |x 1662-8128 |
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