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Elevated NK-mediate...
Elevated NK-mediated lysis of Raji and Daudi cells carrying fixed iC3b fragments
- Artikel/kapitelEngelska1989
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LIBRIS-ID:oai:DiVA.org:lnu-1108
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https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-1108URI
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https://doi.org/10.1016/0008-8749(89)90258-XDOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-265388URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
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Raji and Daudi cells were opsonized with C3b, iC3b and C3d fragments by using purified complement components. The sensitivity of C3-opsonized cells to lysis mediated by low density blood lymphocytes was studied. Raji and Daudi cells carrying C3b or C3d fragments were lysed with similar efficiencies as the nonopsonized cells. The presence of iC3b on the target surface imposed elevated NK sensitivity. The iC3b-mediated enhancement of NK lysis was inhibited when iC3b fragments or rabbit anti-human C3 antibodies were included into the lytic assays. These results indicate that the iC3b fragments fixed on the targets bind to the CR3 on the lymphocytes. Results obtained in immobilized conjugate-lytic assays showed that iC3b-opsonized targets interact more readily with the lymphocytes. This was reflected by the elevated proportion of lymphocytes that were bound to the iC3b-carrying targets. The proportions of conjugates in which target damage occurred were similar with the control and with the iC3b-carrying cells. It seems therefore that opsonization of targets with iC3b leads to recruitment of effector lymphocytes due to contact with their CR3. However, once the effector-target contact is established, the triggering of lytic function does not seem to be influenced by the iC3b/CR3 bridge.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Nilsson, BoUppsala universitet,Institutionen för onkologi, radiologi och klinisk immunologi
(författare)
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Nilsson Ekdahl, KristinaUppsala universitet,Institutionen för onkologi, radiologi och klinisk immunologi,The Blood Centre, University Hospital, Uppsala(Swepub:lnu)nnikr
(författare)
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Eggertsen, G
(författare)
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Yefenov, E
(författare)
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Klein, E
(författare)
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Uppsala universitetInstitutionen för onkologi, radiologi och klinisk immunologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Cellular Immunology119:2, s. 459-4690008-87491090-2163
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