Adenovirus infection induces loss of HLA class I and CD3 antigens, but does not induce cell surface presentation of the La (SS‐B) autoantigen

SUMMARY Antibodies to the RNA polymerase III transcription termination factor La arc frequently found in the serum of patients with various autoimmune diseases. The mechanisms by which autoimmune responses are evoked remain largely obscure, hut the presentation of autoantigens on the cell surface du...

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Veröffentlicht in:Clinical and experimental immunology 1994-06, Vol.96 (3), p.395-402
Hauptverfasser: PEEK, R., WESTPHAL, J. R., PRUUN, G. J. M., KEMP, A. J. W., VENROOIJ, W. J.
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Sprache:eng
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Zusammenfassung:SUMMARY Antibodies to the RNA polymerase III transcription termination factor La arc frequently found in the serum of patients with various autoimmune diseases. The mechanisms by which autoimmune responses are evoked remain largely obscure, hut the presentation of autoantigens on the cell surface during stress conditions has been reported as a possible factor. In this study we analysed the effects of adenovirus infection on the binding of anti‐La antibodies to the surface of several human cell lines and on the levels of the membrane‐expressed glycoproteins HLA class I. CD44 and (hcCD3 complex. In addition, we studied the relative amount and the intracellular distribution of the La protein as well U its association with the major species of non‐coding virus‐associated (VAI) RNA. While immunofluorescence patterns revealed a redistribution and possibly cell surface expression of the L a protein during infection, this could not be confirmed by other techniques. In contrast, surface levels of HLA class I proteins and CD3 complex were severely affected. The data suggest that the subcellular distribution of the La protein is not detectably influenced by adenovirus infection.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.1994.tb06041.x