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PubMed1977

Determination of cryoglobulins as lipoprotein-autoantibody immune complexes and antigenic determinants against antilipoprotein autoantibody.

Serum IgG-antilipoprotein-autoantibody activity (at 4 degrees C) of a plane xanthoma patient was shown by double-immunodiffusion method. Cryoglobulins in the serum were dissociated to polyclonal IgG and alpha- and beta-lipoproteins by acidification and were reconstructed by neutralization. IgG fraction of the cryoglobulins precipitated with lipoproteins. The cryoglobulins were thus demonstrated to be immune complexes of polyclonal IgG-antilipoprotein-autoantibody and both alpha- and beta-lipoproteins. A part of the lipoprotein-autoantibody immune complexes was not cryoprecipitable. Antigenic determinants for the autoantibody existed in the lipid moieties of lipoproteins, in contrast to the apoproteins which determined the specificity to heteroimmune antilipoprotein antibody. The presence of more than nine different antigenic determinants against the autoantibody indicated that lipoproteins were immunologically heterogeneous depending upon the lipid moieties. Lipoproteins reactive with the autoantibody varied quantitatively in normal individuals and were not detected in a primary hyper-beta-lipoproteinaemia patient and in a primary biliary liver cirrhosis patient with much lipoprotein-X. The absence of antigenicity in the two patients' sera is most likely caused by abnormal lipid moieties of lipoproteins.

Adult↗

PubMed1978

Diagnostic specificity of autoantibodies. II. Clustering of autoantibodies--role in diagnosis and in comparison to E--and EAC-RFC peripheral blood profiles and immunoglobulin levels.

Clustering of ANA and SMA was evaluated in patients with various internal diseases as a pattern of autoantibody formation. SMA was found in ANA positive patients with chronic hepatitis, undefined collagenoses and autoallergic thyroid diseases significantly more frequently, than in patients without any autoallergic disorders. The incidence of SMA in ANA positive cases with SLE and RA did not exceed their predictable by chance incidence. It was not found that clustering of autoantibodies is correlated with the E and C lymphocyte receptor abnormality as compared to the control group. The lowest count of E-RFC was found in SLE cases which differed significantly in this respect from the control group and also from chronic vasculitis cases. The clustering of autoantibodies is not correlated with hyperimmunoglobulinemia.

Antibodies, Antinuclear↗

PubMed1978

Binding affinity of human autoantibodies: studies of cryoglobulin IgM rheumatoid factors and IgG autoantibodies to albumin.

The binding affinity of cryoglobulin IgM rheumatoid factors (RF) for human IgG and of human IgG anti-albumin autoantibodies for HSA was measured by the molecular sieving technique. The binding affinities of the two autoantibodies were consistently low (10(4)-10(5) 1/M) as compared to the affinities of corresponding hyperimmune animal antibodies (10(6)-10(8) 1/M). The findings were discussed in relation to theories on human autoimmunity. The existence of strict autotolerance at the T cell level and of autoreactivity at the low affinity B cell level was considered to be best compatible with the findings of this study and with the major known facts of autoimmunity.

Antibodies↗

PubMed1977

Reaction of human smooth muscle autoantibody with gastric parietal cells: a pitfall in the diagnosis of parietal cell autoantibody.

Thirteen smooth muscle antibody (SMA) sera obtained from patients with active chronic hepatitis were examined for immunofluorescence reactivity with gastric mucosal cells. Eight out of 13 sera stained the cytoplasm of gastric parietal cells in a pattern indistinguishable from that obtained with parietal cell autoantibody (PCA). The staining reaction was localised to parietal cells by the demonstration that the same cells stained with both SMA and PCA in double immunofluorescent tests. The SMA staining intensity for parietal cells was weaker than that for smooth muscle. Specificity of the staining reaction for actin was established by the observation that parietal cell staining by SMA was inhibition by serum absorption with skeletal muscle F-actin but not by a microsomal fraction derived from gastric mucosa.

Anemia, Pernicious↗

PubMed1978

Diagnostic specificity of autoantibodies. III. Age related changes in appearing autoantibodies serum IgD levels and their association with peripheral blood lymphocyte profiles.

Comparisons made between old and young people depicted the increase with aging in ANA and thyroid antibody incidence. In contrast to these antibodies SMA were frequently seen in young women. Also in women serum IgM levels were higher as compared to men. Conversely serum IgD levels were higher in men; both these differences were seen in the young group only. Proportions and numbers of E-RFC were significantly reduced in the older group of people as compared to the values of the younger group. Interestingly, the autoantibodies appearing were correlated in women with a lower percentage of E-RFC. Also in women low IgD levels were associated significantly with higher percentage of E-RFC.

Adult↗

PubMed2022

Heterogeneity of Acetylcholine Receptor Autoantibody-Mediated Complement Activity in Patients With Myasthenia Gravis.

BACKGROUND AND OBJECTIVES: Autoantibodies targeting the acetylcholine receptor (AChR), found in patients with myasthenia gravis (MG), mediate pathology through 3 mechanisms: complement-directed tissue damage, blocking of the acetylcholine binding site, and internalization of the AChR. Clinical assays, used to diagnose and monitor patients, measure only autoantibody binding. Consequently, they are limited in providing association with disease burden, understanding of mechanistic heterogeneity, and monitoring therapeutic response. The objective of this study was to develop a cell-based assay that measures AChR autoantibody-mediated complement membrane attack complex (MAC) formation. METHODS: An HEK293T cell line-modified using CRISPR/Cas9 genome editing to disrupt expression of the complement regulator genes (CD46, CD55, and CD59)-was used to measure AChR autoantibody-mediated MAC formation through flow cytometry. RESULTS: Serum samples (n = 155) from 96 clinically confirmed AChR MG patients, representing a wide range of disease burden and autoantibody titer, were tested along with 32 healthy donor (HD) samples. AChR autoantibodies were detected in 139 of the 155 (89.7%) MG samples through a cell-based assay. Of the 139 AChR-positive samples, autoantibody-mediated MAC formation was detected in 83 (59.7%), whereas MAC formation was undetectable in the HD group or AChR-positive samples with low autoantibody levels. MAC formation was positively associated with autoantibody binding in most patient samples; ratios (mean fluorescence intensity) of MAC formation to AChR autoantibody binding ranged between 0.27 and 48, with a median of 0.79 and an interquartile range of 0.43 (0.58-1.1). However, the distribution of ratios was asymmetric and included extreme values; 16 samples were beyond the 10-90 percentile, with high MAC to low AChR autoantibody binding ratio or the reverse. Correlation between MAC formation and clinical disease scores suggested a modest positive association (rho = 0.34, p = 0.0023), which included a subset of outliers that did not follow this pattern. MAC formation did not associate with exposure to immunotherapy, thymectomy, or MG subtypes defined by age-of-onset. DISCUSSION: A novel assay for evaluating AChR autoantibody-mediated complement activity was developed. A subset of patients that lacks association between MAC formation and autoantibody binding or disease burden was identified. The assay may provide a better understanding of the heterogeneous autoantibody molecular pathology and identify patients expected to benefit from complement inhibitor therapy.

Autoantibodies↗

PubMed1977

Disappearance of IgG2B autoantibodies associated with recovery from anaemia.

Mice immunized with cross-reacting rat erythrocytes develop autoimmune haemolytic anaemia as indicated by haematological data and erythrocyte autoantibodies. With continued immunization the mice recover haematologically but remain Coombs' positive. Coombs' tests were performed using monospecific antisera to determine whether the recovery from anaemia was associated with a change in the class or subclass of the autoantibodies produced. In both splenectomized mice and in unsplenectomized mice the following subclass of erythrocyte autoantibodies were present: IgG1, IgG2A, IgG2B. IgA autoantibodies were not detected and IgM autoantibodies were only detected in splenectomized mice 1-3 weeks after the IgG autoantibodies had appeared. After six immunizations the frequency of IgG2B autoantibodies decreased and by the tenth immunization and thereon, IgG2B autoantibodies were not detected. It is proposed from these results that the anaemia is caused by IgG2B autoantibodies and the the sudden exacerbation in the anaemia that occurs in splenectomized mice is due to the production of IgM autoantibodies.

Anemia, Hemolytic, Autoimmune↗

PubMed2026

Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza: an observational case-control study.

BACKGROUND: The determinants of the species barrier preventing human infections with avian influenza A viruses (IAV) are incompletely understood. We previously identified loss-of-function variants of the interferon-regulated antiviral factor MxA as a genetic factor for increased susceptibility to infections with the H7N9 subtype. Given the central role of type I IFNs (IFN-I) in antiviral defence, we hypothesised that IFN-I-neutralising autoantibodies may similarly predispose to zoonotic H7N9 infection. METHODS: In this observational case-control study, serum samples collected between 2013 and 2017 from 199 Chinese patients with laboratory-confirmed H7N9 infection and 531 healthy, uninfected controls (269 poultry workers, 262 close contacts) were screened for IgG autoantibodies binding IFNα2, IFNβ1b, or IFNω using a multiplex bead-based assay. Positive samples were tested for IFN-neutralising activity in a luciferase-based reporter assay. To confirm their ability to block IFNα2-mediated antiviral activity, selected samples (n = 19) were analysed in IAV infection experiments. Associations between age, sex, H7N9 case status, case fatality, and the presence of neutralising autoantibodies were evaluated by logistic regression. Available whole-genome sequencing data from 26 individuals with neutralising autoantibodies were screened for variants in genes linked to IFN-I autoimmunity. FINDINGS: Neutralising autoantibodies against at least one IFN-I were detected in 19.1% (38/199) of patients but in only 1.1% (6/531) of controls, consistent with published general population data. Most patient sera targeted IFNα2 and/or IFNω (35/199), and 18.1% (36/199) neutralised even high IFN-I concentrations of 1-10 ng/ml. The presence of neutralising autoantibodies was associated with 8.2- to 25.3-fold higher odds of H7N9 infection (p < 0.0001), depending on antibody specificity and reference group. Autoantibody prevalence increased significantly with age in patients (44.8% ≥70 years; OR = 1.05; 95% CI 1.02-1.07; p = 0.0001), but was not associated with sex (OR for males vs. females = 0.52; 95% CI 0.23-1.14; p = 0.106). All selected sera containing neutralising autoantibodies blocked IFNα2-induced antiviral activity in cell culture. No known genetic predisposition for IFN-I autoimmunity was identified. INTERPRETATION: Our findings suggest that IFN-I-targeting autoimmunity is associated with susceptibility to zoonotic IAV infection with the H7N9 subtype, and possibly also other subtypes, including panzootic H5N1. Given the ease of implementation, screening for anti-IFN-I autoantibodies could be readily integrated into surveillance or targeted testing. This could be relevant in environments with increased exposure to zoonotic IAVs. FUNDING: Shenzhen Medical Research Fund, National Natural Science Foundation of China, Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences, Guangdong Provincial Science and Technology Program, Program for Youzuzhikeyan of Shenzhen University, German Research Foundation, Swiss National Science Foundation.

Humans↗

PubMed1979

Impaired regulation of erythrocyte autoantibody production after splenectomy.

C3H mice were given 4 i.p. injections, eac of 2 X 10(8) WAG rat RBC, at weekly intervals. The production of erythrocyte autoantibodies elicited by the cross-reacting rat RBC was assessed using the average direct Coombs' test (DCT) score. Autoantibody production reached higher levels and persisted significantly longer in mice splenectomized 15 days before the first injection of rat RBC. This increased production of autoantibodies was not prevented by injecting each splenectomized mouse i.v. with 5 X 10(7) syngeneic spleen cells immediately after splenectomy. Similarly, splenectomy of mice already DCT+ significantly prolonged autoantibody production which was not prevented by injections of 10(8) cells prepared from the spleens removed at splenectomy. Transfer of spleen cells from mice already DCT+ to mice before the injections of rat RBC were started in the recipients caused a significant reduction in the amount of RBC autoantibodies produced. This suppression of autoantibody production was greater in unsplenectomized mice than in splenectomized mice. The results show that the spleen is involved in the regulation of these erythrocyte autoantibody responses. It is hypothesized that, in addition to the cellular component of the spleen, the splenic architecture and/or environment contributes to the regulation of autoantibody responses.

Animals↗

PubMed1976

Anti-Wrb, and other autoantibodies responsible for positive direct antiglobulin tests in 150 individuals.

Eluates from the red blood cells (and sera whenever free autoantibody was present) of 150 individuals with positive direct antiglobulin tests, have been studied for antibody specificity. Of 87 patients with AIHA, 64 had autoantibodies reacting with all red cell samples including Rhnu11. Of these 64 anti-d1 autoantibodies, two were, and 32 contained, auto-anti-Wrb. Of 33 patients being treated with alphamethyldopa, who had developed positive direct antiglobulin tests, 23 had anti-d1 autoantibodies four of which contained auto-anti-Wrb. Of 30 haematologically normal donors with positive direct antiglobulin tests, 23 had anti-d1 autoantibodies, two of which were, and six of which contained, auto-anti-Wrb. The full specificities of autoantibodies, other than anti-Wrb and anti-d1, in the 150 patients are described, as are the natures of the protein red cell coatings that caused the positive direct antiglobulin tests. The presence of free serum autoantibody as a correlate of the three clinical conditions is reported. Several observations on auto-anti-Wrb are documented. The antibody can cause gross red cell destruction in vivo, but can be benign on other occasions; it occurs with approximately the same frequency in AIHA patients and "normal" donors with positive direct antiglobulin tests, but in fewer patients with alphamethydopa induced positive direct antiglobulin tests; it does not activate complement in vivo; and finally it may eventually provide a clue to the aetiology of AIHA.

Anemia, Hemolytic, Autoimmune↗

PubMed1979

Smooth muscle autoantibodies and autoantigens.

Smooth muscle autoantibody (SMA) was first found in the sera of patients with chronic active hepatitis and subsequently in the sera of patients with other autoimmune liver diseases, viral infections, certain cancers, heroin addicts and female infertility. SMA from patients with chronic active hepatitis reacts with many muscle and 'non-muscle' tissues while SMA from patients with other diseases usually reacts only with smooth muscle. These differences in immunofluorescent staining reactions suggest that SMA is a heterogeneous group of autoantibodies reactive with different smooth muscle autoantigens. As further evidence for this are findings that broad-reacting SMA can be absorbed out by actin, whereas autoantibodies reactive only with smooth muscle cannot, and that different SMAs give different immunofluorescent staining patterns using fibroblasts in tissue culture. Such staining patterns correspond to reactivity with either microfilaments, microtubules or intermediate filaments, ubiquitous cytoplasmic structures which make up the 'cytoskeleton'. Autoantibodies to actin-like microfilaments appear specific for chronic active hepatitis, autoantibodies to microtubules occur in infectious mononucleosis whereas autoantibodies to intermediate filaments occur in infectious hepatitis, chickenpox, measles and mumps. Predictably, future studies will show that presence of SMA with specificities for other proteins in the three types of cytoplasmic filaments, and given more information on antigenicity of the proteins and pathogenicity of the corresponding autoantibodies.

Actins↗

PubMed1978

Autoantibodies in aged individuals.

Authors determined in 282 individuals autoantibodies in 132 T and B lymphozytes. Theirs results were as follows: 1. The frequency of the presence of autoantibodies increases with age. 2. In the presence of autoantibodies the absolute T and B lymphocyte counts of aged persons markedly decrease; the absolute T and B lymphozyte counts of young adult people do not change by existing autoantibodies. 3. There is a significant difference between the absolute T cell counts of aged and young adult age groups, both age-groups having autoantibodies. 4. Comparing the frequency of occurence of autoantibodies in aged healthy persons and in aged ones with cardiovascular changes and being in the habit of smoking and consuming alcohole, respectively, a significant difference could be demonstrated; in the latter group the frequency was much higher.

Age Factors↗

PubMedDate not supplied

A "normal" individual with a positive direct antiglobulin test: case complicated by pregnancy and unusual autoantibody specificity.

A "normal" individual with a positive, direct antiglobulin test is described. In common with many other "normal" persons in whom a similar finding has been made, there was no evidence of an increased rate of in vivo red blood cell destruction in this patient. The patient successfully completed a pregnancy during the time that detailed serologic studies on her autoantibodies were being performed. Although the maternal autoantibodies were demonstrable in both an eluate made from the red blood cells of her newborn infant, and in the cord serum, there was no reason to believe that the antibodies caused red blood cell destruction in the infant. The case was of further interest because of the specificities of some of the autoantibodies. Although the mother and child were both C-negative, eluates from their red blood cells contained what ostensibly appeared to be anti-C. Studies that showed that the antibody could be totally adsorbed with C-negative, as well as C-positive red blood cells, proved that this was another example of an autoantibody mimicking an alloantibody. Although this autoantibody appeared initially to have anti-C specificity it was eventually shown to be more closely related to anti-Hr or anti-Rh34, than to anti-C.

Adult↗

PubMed2026

Pathogenic properties of myasthenia gravis AChR autoantibodies associate with clinical response to efgartigimod.

BACKGROUND: Efgartigimod, a neonatal Fc receptor (FcRn) blocker, effectively reduces total IgG, including pathogenic acetylcholine receptor (AChR) autoantibodies in myasthenia gravis (MG); however, clinical responses vary. To investigate this variability, we studied how efgartigimod impacts AChR-specific autoantibody profiles and associated pathogenic mechanisms, including complement activation, AChR internalisation and ACh-binding site blockade. METHODS: Serum samples (N=150) were sourced from 50 AChR autoantibody-positive generalised MG patients participating in the phase 3 ADAPT study, randomised to receive efgartigimod (N=40) or placebo (N=10) in cycles of 4-weekly infusions. Samples were collected at baseline, day 29 and day 57 during the first cycle. Live cell-based assays quantified AChR-specific IgG subclasses and isotypes and assessed their capacity to mediate pathomechanisms. RESULTS: Efgartigimod decreased all detectable AChR-specific IgG subclasses. At baseline, AChR autoantibody-mediated C3b deposition, AChR internalisation and ACh-binding site blockade were detected in 42 (84%), 41 (82%) and 10 (20%) patients, respectively. After 4-weekly infusions of efgartigimod, the magnitude of all three pathomechanisms was significantly decreased. However, the extent of this reduction varied across individuals. Double responders on both MG-activities of daily living and quantitative MG scores demonstrated a greater reduction in complement activity and AChR internalisation compared with patients who responded on only one score or were double non-responders. In addition, efgartigimod reduced IgG-dependent IgM binding to AChR. CONCLUSIONS: These findings suggest that clinical efficacy may be more closely associated with functional modulation of the AChR-specific autoantibodies than with their absolute quantity alone. These results support the evaluation of mechanistic pathway monitoring as a potential strategy to predict or guide efgartigimod treatment response.

Humans↗

PubMed1975

[Anti-lipoprotein autoantibodies with hypolipidemia in infectious rheumatism].

Presence of anti-lipoprotein activity, a new serological finding in inflammatory rheumatoid disease, has been established in sera and synovial fluids of 20 patients, among which were 6 cases of ankylosing spondylitis. In 18 of the patients, sera were negative for rheumatoid factor. Anti-lipoprotein activity can best be demonstrated by the hemagglutination technique. The binding activity is directed against autologous as well as homologous, however not against heterologous HDL and LDL. It has no specificity for Ag factors. Anti-LDL activity can also be demonstrated by means of double-diffusion tests, whereas no agar-precipitation has been noticeable using HDL as the antigen. Lipoprotein binding-activities were shown to be localized in the Fab fragments of IgG and, in 2 of the cases, also in IgA. We therefore assume that the underlying mechanism of the antilipoprotein activity is auto-immunization, despite of the fact that neither activation of complement nor a stoichiometric character of the binding reaction could be ascertained. Because hemagglutination and immunoprecipitation tests, respectively, were postive with apo-HDL und apo-LDL too, we consider the apo-protein to carry the antigenic site of the reaction. Sera with anti-lipoprotein autoantibodies from patients with chronic rheumatoid disease also presented another pecularity, i.e., a significant decrease of total lipids, cholesterol, and other components of the lipid spectrum. In patients with paraproteinemia, a similar combination of lipoprotein-binding activity and hypolipidemia or hypocholesterolemia was discussed in a previous paper. Regarding the pathogenesis of hypolipidemia or hypocholesterolemia in our patients with rheumatoid disorders, results of LDL turnover studies were indicative for an increase of the lipoprotein catabolism in the presence of anti-lipoprotein autoantibodies, together with a shift of the intra-extravascular distribution toward the intravascular pool. We assume the increased lipoprotein catabolism in these cases to be due to a trapping of lipoproteins by autoantibodies, and to accelerated degradation of these immune complexes. From a practical point of view, it may be of clinical importance that this new serological finding has been observed mainly in patients with chronic rheumatoid disease lacking a rheumatoid serum factor, and was frequently found in patients with ankylosing spondylitis (6 out of the 20 cases). As a screening method, we recommend systematic determinations of the total lipids and of serum cholesterol in all patients with inflammatory rheumatoid disease. In cases with low levels of total lipids and cholesterol, respectively, it may be useful to search for anti-lipoprotein autoantibodies using the hemagglutination method. Results are reported from some preliminary experiments on animals elicitation of an arthritis by means of intra-articular injections of autologous apo-HDL and apo-LDL, and demonstration of autoantibodies against HDL and LDL).

Adult↗

PubMed1978

Delineation of spontaneous erythrocyte autoantibody responses of NZB and other strains of mice.

Four anti-erythrocyte autoantibody responses (anti-X, anti-HB, anti-HOL, and anti-I) that occur spontaneously in mice have been characterized with regard to antigenic specificities, predominant immunoglobulin class, and pathogenetic importance. Each autoantibody response exhibits specificity for an independent erythrocyte membrane autoantigen (X, HB, HOL, or I) or a soluble analogue (SEA-X or SEA-HB) present in the plasma. The anti-X response, unique to NZB mice, is directed to a normally exposed murine erythrocyte autoantigen, whereas the anti-HB response is directed to a cryptic erythrocyte autoantigen exposed by limited enzymatic cleavage of the membrane. The anti-I response also is directed to a cryptic but distinct autoantigen, and anti-HOL autoantibodies react with an erythrocyte autoantigen located at the cytoplasmic surface of the membrane. Analysis of the predominant immunoglobulin class of each of the autoantibodies has demonstrated that anti-HB and anti-I antibodies are predominantly of IgM class, whereas anti-X and anti-HOL antibodies are IgG immunoblobulins. Only anti-X and anti-HB autoantibodies are recovered from Coombs' positive erythrocytes from NZB mice and erythrocytes with surface C3 are detected only in NZB mice greater than 9 months of age. These data suggest that only the anti-X and anti-HB responses are pathogenetically implicated in the autoimmune hemolytic anemia of NZB mice.

Animals↗

PubMed1977

Renal transplantation and B-cell cross-matches with autoantibodies and alloantibodies.

Of 51 cadaveric kidneys transplanted between June, 1976, and June, 1977, 18 were transplanted in the presence of a positive cross-match against the donor's B lymphocytes. 11 of these positive cross-matches were due to alloantibodies and 7 due to autoantibodies. Autoantibodies were defined not only on the basis of autoreactivity with B lymphocytes but also by their absent or restricted reactivity with lymphocytes from patients with chronic lymphocytic leukaemia. Transplants in 8 of 11 patients with a positive alloantibody-B-cell cross-match and in 6 of 7 patients with a positive autoantibody-B-cell cross-match were successful at 3 months. These success-rates were no different from those found in patients with a negative B-cell cross-match. Thus, renal allografts may be performed with a reasonable assurance of success in the presence of a positive B-cell cross-match whether due to autoantibodies or to alloantibodies.

Antibodies, Heterophile↗

PubMed1978

Autoimmune granulocytopenia: the detection of granulocyte autoantibodies with the immunofluorescence test.

Neutropenia may be caused by neutrophil autoantibodies. The detection of such antibodies has always been difficult. Recently, we developed a sensitive indirect immunofluorescence technique applicable to granulocytes which proved to be of value in the detection of granulocyte alloantibodies. We have now used this method to investigate the serum and cells of 29 patients with idiopathic or secondary neutropenia. In four patients neutrophil-antigen-specific autoantibodies were detected in the serum and the patient's own granulocytes showed direct fluorescence. Furthermore, differences in the immunoglobulin composition and the temperature of optimal activity of the autoantibodies were found. Direct fluorescence was also demonstrated with the granulocytes from five other neutropenic patients and with the granulocytes from five non-neutropenic patients mainly with infectious disease. However, no granulocyte antibodies could be eluted or shown to be present in the serum. This indicates that a positive direct granulocyte fluorescence test may not be considered as proof that autoantibodies are present.

Adult↗