Cutting edge: Productive HIV-1 infection of dendritic cells via complement receptor type 3 (CR3, CD11b/CD18)

Zsuzsa Bajtay, Cornelia Speth, Anna Erdei, Manfred P. Dierich

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

In the present study, we demonstrate that macrophagetropic HIV-1 opsonized by complement and limited amounts of anti-HIV-IgG causes up to 10-fold higher productive infection of human monocyte-derived dendritic cells than HIV treated with medium or HIV opsonized by Ab only. Enhanced infection is completely abolished by a mAb specific for the ligand-binding site of CD11b (i.e., α-chain of complement receptor 3, receptor for iC3b), proving the importance of complement receptor 3 in this process. Inhibition of complement activation by EDTA also prevents enhanced infection, further demonstrating the role of complement in virus uptake and productive infection. Since HIV is, even in the absence of Abs, regularly opsonized by complement, most probably the above-described mechanism plays a role during in vivo primary infection.

Original languageEnglish
Pages (from-to)4775-4778
Number of pages4
JournalJournal of Immunology
Volume173
Issue number8
DOIs
Publication statusPublished - Oct 15 2004

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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