摘要:

Immunocompetent mice infected with LDVAG1Adeveloped autoantibodies against Golgi antigen as early as 6-7 days postinfection preceding anti-viral antibodies for nearly a week. The anti-Golgi antibody titres peaked between two and three weeks postinfection independent of the applied virus dose. Already one week postinfection anti-Golgi autoantibodies were prominent in IgG subclasses IgG2a and b. Spleen cells from these mice were fused with myeloma cells and the culture fluids were screened by indirect immunofluorescence for antibodies reactive with the Golgi antigen of normal cultured cells. A panel of cloned stable antibody-producing hybridomas has been obtained. Some antibodies showed broad cross-species reactivity, recognizing similar antigenic determinants in the Golgi region of mouse, rat and other mammalian cells and also in avian and piscine cells, whereas others recognized determinants in this cell compartment only in mammalian cells and one recognized Golgi antigen only in particular murine tumor cells. From 19 Golgi antibody producing hybridomas 3 secreted IgM-antibodies, 10 synthesized autoantibodies of the subclass IgG2a and 6 of IgG2b. Applied in immunoelectron microscopy mABs decorated the Golgi organelle. A considerable amount of LDVAGIA-induced hybridomas produced antibodies against conserved antigens associated with the cytoskeleton, mitochondria, and the nucleus. LDV-induced monoclonal anti-Golgi antibodies decorated the Golgi area in LDV- and mock-infected macrophages. However, cytoplasmic fluorescence characteristic for LDV-infected cells was not observed indicating that the anti-Golgi autoantibodies do not cross-react with the virus.

ISSN:0891-6934    

DOI:10.3109/08916938909014684

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

The clinical, biochemical, histopathological and immunological features of 30 cases of clometacin-induced hepatitis are described. The age range of the patients was 32-84 years with a notable female predominance of 29:1. The hepatitis was highly cytolytic with high values of transaminases but with little or no cholestasis. Gammaglobulins were higher than 18 g/1 in 73% of the cases. 25 liver biopsies were performed and showed acute hepatitis with a predominant centrilobular necrosis in 17; chronic aggressive hepatitis was noted in 8 cases but 1 showed concomitant cirrhotic changes. Anti-tissue antibodies were looked for in all cases. Anti-smooth muscle antibodies of anti-actin cable type (titre 1/80 to 1/2, 560) were detected in 19 cases, anti-nucleus antibodies in 16 cases which were associated to the former in 14 cases. The above findings show that clometacin produces a hepatitis syndrome quite akin to autoimmune chronic active hepatitis (lupoid hepatitis) and to the hepatopathy induced by oxyphenisatin.

ISSN:0891-6934    

DOI:10.3109/08916938909014685

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Balb/c mice were immunized with homologous heart in complete Freund's adjuvant to induce autoimmune myocarditis. The myocarditis was characterized by lymphomononuclear infiltration, electrocardiographic abnormalities and antimuscle antibodies by indirect immunofluorescence. In this paper, we demonstrate that the IgG present in autoimmune myocarditis mice is able to bind toβ-adrenoreceptors of the heart and also induce a biological effect inhibiting the contractile action of exogenous norepinephrine. Auto-immune IgG inhibited the binding of (3H)-dyhidroalprenolol to aβ-adrenergic receptor of purified myocardial membranes behaving as non-competitive inhibitor. This IgG also exerted a non-competitive inhibition upon the mechanical effect of exogenous norepinephrine. The recognition appears to be organ specific, because the autoimmune myocarditis IgG did not bind toβ-lymphocyte, lung and fat adrenoreceptors. The autoimmune IgG inhibited the stimulatory action of isoproterenol on cAMP levels, behaving as aβ-adrenergic antagonist.

ISSN:0891-6934    

DOI:10.3109/08916938909014686

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

A sensitive and simple sandwich enzyme immunoassay (EIA) using a dot microfiltration apparatus has been developed for the measurement of immunoglobulin M (IgM) concentrations in cerebrospinal fluid (CSF). The lower detection limit was 0.5μg/dl. We applied this method to the testing of 200 CSF samples with normal concentrations of albumin, IgG and total protein, and normal cell counting. The non-parametric 2.5 and 97.5 percentile limits of IgM and the IgM index were 6.1-64.3μg/dl and 0.012-0.063, respectively. We also applied this method to the testing of samples from 11 cases of multiple sclerosis (MS) and 15 cases of Guillain-Barrésyndrome (GBS). High values for IgM and the IgM index were observed in 18.2% and 9.1% of MS, respectively and in 66.6% and 20.0% of GBS, respectively.

ISSN:0891-6934    

DOI:10.3109/08916938909014687

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Monoclonal anti-Sm antibody, a specificity directed against a constituent of nuclear ribonucleoprotein and considered to be a marker for systemic lupus erythematosus (SLE), was tested for its ability to react with four other rheumatic disease antigens of known enzymatic activity. No binding of the antibody was observed in radioimmunoassays with immobilized protein kinase Nil, po!y(A) polymerase, or topoiso-merase I. In contrast, anti-Sm antibody did react with RNA polymerase I. Under conditions of antibody excess, anti-Sm was determined to bind RNA polymerase I on an equimolar basis, indicating that the polymerase posesses a single epitope recognized by the anti-Sm antibody. Addition of the anti-Sm antibody toin vitrotranscription reactions resulted in inhibition of RNA polymerase I activity but had no effect on the reaction catalyzed by RNA polymerase II. When the subunits of RNA polymerase I were separated by polyacrylamide gel electrophoresis under denaturing conditions and incorporated individually into the radioimmunoassay. anti-Sm antibody bound only to the sixth polymerase polypeptide (Mr, 21,000). These data establish an immunological relationship between two important rheumatic disease antigens and help explain the apparent diversity of the autoimmune response in murine and human SLE.

ISSN:0891-6934    

DOI:10.3109/08916938909014688

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

We have characterized thyroid microsomal antigen (M-Ag) prepared from Graves' and normal thyroid tissues using 100,000×g thyroid membrane fractions in enzyme-linked immunosorbent assays with pooled polyclonal human sera containing high titers of antibody to M-Ag. A ten-fold parallel increase in dose inhibition potencies occurred with M-Ag preparations from Graves' as compared to normal thyroid tissue. The M-Ag preparations wre further evaluated by SDS-polyacrylamide gel electrophoresis and proteins visualized by Western blot using high titer microsomal antibody (M-Ab) sera (n = 2) devoid of thyroglobulin antibody activity. We found discrete 100 kD relative molecular mass bands in Graves' M-Ag preparations (n = 3) under nonreducing conditions which were only poorly resolved in normal thyroid M-Ag (n = 3) using up to 100μg of protein per lane.The cellular localization of M-Ag was then investigated using the avidin-biotin-peroxidase technique on frozen sections of Graves' and normal human thyroid tissue with a murine monoclonal antibody reactive with human M-Ag and thyroid peroxidase. M-Ag reactivity was similar in both Graves' and normal thyroid tissues and localized to the entire follicular cell membrane with more intense staining occurring on the inner follicular cell membrane. This was in contrast to follicular cell staining for HLA-DR antigen which was present in 6 of 10 Graves' tissues examined and absent in normal thyroid tissue. Staining for HLA-DR antigen also occurred on the follicular cell surface membrane with occasional enhancement at the thyrocytc apical cell membrane.We conclude: a) M-Ag is induced approximately 10—fold in Graves' thyroid tissue and can be objectively quantified in ELISA systems, 2) There were no detectable qualitative differences between M-Ag from Graves' and normal thyroid tissue, and 3) HLA-DR antigen was detected on 60% Graves' tissues in a cell surface distribution similar to that observed for M-Ag in both Graves' and normal tissues.

ISSN:0891-6934    

DOI:10.3109/08916938909014689

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

CNS demyelinating inflammatory disease can be a multifactorial process mediated by cellular and antibody-mediated immune processes. Myelin basic protein (MBP)-specific T cells and pathogenic 8-18C5 antibody, specific for a myelin/oligodendrocyte glycoprotein (MOG), a minor component of CNS white matter, can coexist in rats without triggering disease. However, transfer of activated MBP-specific T-cells followed by the injection of 8-18C5 antibody resulted in hyperacute disease progression and CNS demyelination. Transfer of activated T cells specific for an irrelevant antigen or transfer of activated but irradiated encephalitogenic T cells did not induce disease in the presence of 8-18C5 antibody. When needle lesions were induced in brains of 8-18C5 antibody treated rats, no enhancement of demyelination was seen around the needle track. Thus, accessibility of the brain parenchyma to 8-18C5 antibody was not sufficient to induce local demyelination. Therefore, it appears that activated encephalitogenic T cells are involved in initiating the 8-18C5 antibody-mediated demyelinating process.

ISSN:0891-6934    

DOI:10.3109/08916938909014690

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor