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Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons
Author(s) -
ATTA M. S.,
IRVING W. L.,
POWELL R. J.,
TODD I.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb02287.x
Subject(s) - mhc class i , biology , mhc class ii , major histocompatibility complex , interferon , virology , virus , mhc restriction , immunology , microbiology and biotechnology , antigen
SUMMARY Certain viruses are known to modulate the cellular expression of MHC molecules. We have investigated whether reovirus types 1 or 3 can alter the normal MHC molecule expression on cultured human thyroid follicular cells (TFC). Primary TFC cultures were established from eight human thyroid donors and MHC class I and II expression was assessed by indirect immunofluorescence microscopy. Both types of reovirus enhanced MHC class I expression on TFC from all thyroid donors. Class II MHC protein was strongly induced by type 1 reovirus on TFC from one donor, while weak induction of expression, by either reo‐1 or reo‐3 virus, was noted on the TFC of five other donors. Studies on the mechanism(s) of MHC class I hyperexpression showed that mouse MoAb against the type 3 reovirus haemagglutinin (anti‐HA3) reduced the ability of the virus to induce hyperexpression of class I MHC molecules on TFC. However, supernatant harvested from type 3 reovirus‐infected TFC cultures maintained its ability to enhance class I expression after incubation with anti‐HA3. Moreover, adding rabbit anti‐sera lo interferon‐alpha (IFN‐α) or IFN‐β inhibited the increased class I MHC expression on TFC by both types of reovirus. These data suggest that reoviruses (types 1 and 3) can enhance MHC class I on cultured TFC. The mechanism of MHC class I enhancement is most probably through the release of IFN‐α and IFN‐β.

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