SUMMARYThe IgG subclass specificity of Fc receptor(s) induced on cells by infection with human cytomegalovirus (HCMV) was studied in a binding assay by using infected cells and purified iodinated IgG of various subclasses from HCMV seronegative healthy adult donors. All four human IgG subclasses bound to HCMV-infected cells, with the following relative magnitudes: IgG1 t> IgG4 > IgG2 > IgG3. The IgG subclass specificity of the Fc receptor was further analysed in an inhibition assay by using fragments prepared from purified human IgG by papain digestion, and using unlabelled subclass proteins. Fc but not Fab fragments inhibited the binding of 125I-labelled human IgG to HCMV-infected cells. The biological role of the Fc receptor in HCMV infection is discussed.
Synovial fluid aspirated from 34 patients with symptomatic rheumatoid arthritis (RA) was evaluated for the presence of human cytomegalovirus (CMV) genomic material using polymerase chain reaction (PCR), and for levels of interleukin 8 (IL-8) and IL-6 using enzyme-linked immunoadsorbence assay. IL-8 and IL-6 levels were significantly higher in CMV DNA-positive RA patients than CMV DNA-negative RA patients and at least 10-fold higher than in both corresponding control groups of patients with osteoarthritis (OA). These findings suggest an association between elevated IL-8 and IL-6 levels and the presence of the CMV genome in RA patients.
We previously reported that rheumatoid factors (RFs) might bear the internal image of Fc gamma-binding proteins (FcBPs) of herpes family viruses, suggesting the possibility that some RFs may be produced as antiidiotypic antibodies to anti-viral FcBP antibodies. Since human cytomegalovirus (HCMV) has been implicated in the pathogenesis of RA, we made an attempt to detect antibodies to 65 KD major HCMV FcBP in sera and synovial fluid from patients with RA. Western blotting was performed using HCMV-infected MRC-5 cell lysate as the antigen. Eleven of 23 patients with RA possessed strong serum antibodies to HCMV-65 KD protein, whereas such antibodies were found in only 2 of 23 normal controls. In the synovial fluid, 10 of 19 RA patients showed anti-HCMV 65 KD reactivity. Pepsin-digested IgG retained anti-65 KD reactivity, indicating that false-positive reaction due to the presence of IgG Fc portion and/or RF was unlikely. 65 KD protein was shown to be different from human heat shock proteins (hsps) using monoclonal antibodies against human hsps. Patients' IgG F(ab')2 also reacted with the 65 KD protein of purified HCMV virion itself. These results support the possibility that some RFs could be produced as antiidiotypic antibodies to anti-viral FcBP antibodies.
The presence of HCMV-infected cells inhibits the killing of mouse tumor cells by adherent PEC in an antibody-dependent cell-mediated cytotoxicity (ADCC) test system. The effect of HCMV-infected cells on ADCC is mediated by the binding of IgG to the Fc receptors of infected cells.
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