Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity

Y. S. Lin, C. F. Lin, Y. T. Fang, Y. M. Kuo, P. C. Liao, T. M. Yeh, K. Y. Hwa, C. C.K. Shieh, J. H. Yen, H. J. Wang, I. J. Su, H. Y. Lei

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19 Citations (Scopus)

Abstract

Both viral effect and immune-mediated mechanism are involved in the pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In this study, we showed that in SARS patient sera there were autoantibodies (autoAbs) that reacted with A549 cells, the type-2 pneumocytes, and that these autoAbs were mainly IgG. The autoAbs were detectable 20 days after fever onset. Tests of non-SARS-pneumonia patients did not show the same autoAb production as in SARS patients. After sera IgG bound to A549 cells, cytotoxicity was induced. Cell cytotoxicity and the anti-epithelial cell IgG level were positively correlated. Preabsorption and binding assays indicated the existence of cross-reactive epitopes on SARS-CoV spike protein domain 2 (S2). Furthermore, treatment of A549 cells with anti-S2 Abs and IFN-γ resulted in an increase in the adherence of human peripheral blood mononuclear cells to these epithelial cells. Taken together, we have demonstrated that the anti-S2 Abs in SARS patient sera cause cytotoxic injury as well as enhance immune cell adhesion to epithelial cells. The onset of autoimmune responses in SARS-CoV infection may be implicated in SARS pathogenesis.

Original languageEnglish
Pages (from-to)500-508
Number of pages9
JournalClinical and Experimental Immunology
Volume141
Issue number3
DOIs
Publication statusPublished - 2005 Sep 1

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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