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PubMed1999

Autoimmune cholangitis and primary biliary cirrhosis--an autoimmune enigma.

AIMS/BACKGROUND: Autoimmune cholangitis/cholangiopathy (AIC) is an enigmatic disease marked by chronic cholangitis, antinuclear antibodies (ANA) and sero-negativity for conventionally detected antimitochondrial antibodies (AMA). We examined whether AIC is a distinct entity, an AMA-negative variant of primary biliary cirrhosis (PBC), or a cholangiopathic variant of autoimmune hepatitis (AIH) by comparing the clinical, laboratory and autoantibody profiles of 21 cases of AIC, 37 cases PBC and 16 cases of AIH from selected Japanese patients. METHODS: The specificities of AMA and ANA were determined by immunofluorescence, immunoblotting and enzyme inhibition assays using various mitochondrial and nuclear autoantigens, and the frequencies for these groups were compared. RESULTS: By clinical, biochemical and histological data, AIC and PBC were similar and both were clearly distinct from AIH. Serologically, by immunofluorescence of AMA and ANA, there was polarisation. By immunoblotting, and notwithstanding the negative test for AMA, a proportion of the AIC sera reacted with the E2 subunits of the 2-oxo-acid dehydrogenase enzyme complexes, but more particularly with the lower molecular weight E2 subunits. The antinuclear reactivity in AIC was with centromere, Sp100 and nuclear pore complex proteins as in PBC, but preferentially with the nuclear pore complex. CONCLUSION: Our results demonstrate that AIC and PBC are similar diseases. However this duo is of interest because, usually, among sets of autoimmune syndromes, differences in serological targetting are matched by differences in clinical presentation: AIC and PBC are an exception to this.

Adult↗

PubMed2004

Presence of systemic autoimmune disorders in patients with autoimmune thyroid diseases.

OBJECTIVE: To evaluate the prevalence of antinuclear antibodies (ANA) in patients with autoimmune thyroid diseases (ATD) and the presence of systemic autoimmune disorders among ANA positive patients with ATD. METHODS: 168 consecutive patients with ATD with positive antithyroid antibodies and 75 healthy subjects were tested for the presence of ANA. ANA positive patients were further evaluated by complete history, physical examination, blood and urine tests, and immunological studies. Patients with subjective xerophthalmia and xerostomia were examined by objective tests. RESULTS: 58/168 (35%) patients with ATD were ANA positive compared with 7/75 (9%) healthy controls (p = 0.001). Of 58 ANA positive patients, 6 (10%) had anti-Ro antibodies, 1 had anti-Ro and anti-La antibodies, 7 (12%) had anti-dsDNA antibodies, and 7 (12%) had medium levels of IgG and/or IgM anticardiolipin antibodies (aCL). No healthy subjects had positive anti-dsDNA, antibodies against the extractable nuclear antigens, or aCL. 5/58 (9%) patients fulfilled the criteria for Sjögren's syndrome (SS). Two patients had features related to systemic lupus erythematosus. No healthy subjects had clinical or laboratory characteristics of systemic autoimmune disorders. CONCLUSION: ANA are detected in 1/3 of patients with ATD. Anti-dsDNA, anti-Ro, and aCL can also be found in ANA positive patients with ATD. SS occurs in about 1/10 of ANA positive patients with ATD.

Adult↗

PubMed1991

Late appearance of thrombotic thrombocytopenic purpura after autoimmune hemolytic anemia and in the course of chronic autoimmune thrombocytopenic purpura: two case reports.

The association between thrombotic thrombocytopenic purpura (TTP) and autoimmune hematological conditions is reported in 2 patients. In a 35-year-old man, acute autoimmune hemolytic anemia (AIHA) was diagnosed in 1960; until 1965 he was free of disease, when he abruptly developed TTP and failed to respond to blood transfusions and corticosteroids. In a 14-year-old girl, autoimmune thrombocytopenic purpura (AITP) was diagnosed in 1981 and treated with corticosteroids and splenectomy. Four years later the patient was admitted with acute catastrophic signs and symptoms of TTP and failed to respond to plasmapheresis and plasma transfusions. The present case reports of associations between AIHA and AITP with TTP support the connection of the latter with abnormalities of the immune system.

Adolescent↗

PubMed1996

Allogeneic hematolymphoid microchimerism and prevention of autoimmune disease in the rat. A relationship between allo- and autoimmunity.

Conventional allogeneic bone marrow transplantation after myeloablation can prevent experimental autoimmunity and has been proposed as treatment for humans. However, trace populations of donor hematolymphoid cells persisting in solid organ allograft recipients have been associated in some circumstances with therapeutic effects similar to replacement of the entire bone marrow. We therefore examined whether inducing hematolymphoid microchimerism without myeloablation could confer the ability to resist mercuric chloride (HgCl2)-induced autoimmunity. Brown-Norway (BN) rats were pretreated with a syngeneic or allogeneic bone marrow infusion under transient FK506 immunosuppression before receiving HgCl2. They were compared with BN rats receiving either no pretreatment (naive) or FK506 alone. Administration of HgCl2 to naive BN rats induced marked autoantibody production, systemic vasculitis and lymphocytic infiltration of the kidneys, liver and skin in all of the animals and a 47% mortality. In contrast, BN rats pretreated with HgCl2-resistant allogeneic Lewis bone marrow and transient FK506 showed less clinical disease and were completely protected from mortality. More specifically, IgG anti-laminin autoantibody production was decreased by 40% (P < 0.05), and there was less histopathological tissue injury (P < 0.005), less in vitro autoreactivity (P < 0.05), less of an increase in class II MHC expression on B cells (P < 0.01), and 22% less weight loss (P < 0.01), compared with controls. Protection from the experimental autoimmunity was associated with signs of low grade activation of the BN immune system, which included: increased numbers of circulating B and activated T cells before administration of HgCl2, and less autoreactivity and spontaneous proliferation in vitro after HgCl2.

Animals↗

PubMed1988

Insulin-dependent diabetes mellitus, myasthenia gravis, pernicious anaemia, autoimmune thyroiditis and autoimmune adrenalitis in a single patient.

Two classical autoimmune polyendocrine deficiency syndromes with heritable tendencies are described, Type 1 diabetes mellitus being associated with the Type 2 polyendocrine deficiency syndrome (Schmidt's syndrome). A man with Type 1 diabetes mellitus is described who developed an unusual combination of five autoimmune conditions (myasthenia gravis, Addisonian pernicious anaemia, adrenalitis and thyroiditis) which did not fit into the Type 1 or Type 2 classical polyendocrine deficiency syndromes. This suggests that the autoantibody, biochemical and haematological screening of affected individuals and their relatives should be extended to anticipate a wider range of potential autoimmune conditions.

Adrenal Gland Diseases↗

PubMed2003

Autoimmunity and geriatrics: clinical significance of autoimmune manifestations in the elderly.

The immune system undergoes continuous morphologic and functional changes throughout the years, and it is now believed that the immune response has its peak function in puberty and gradually decreases with age (immunosenescence). Recent studies in healthy octogenarian patients suggest that the immune system, instead of suffering a generalized deterioration, undergoes a remodelling/readjustment of its major functions. Increase in two contrasting phenomena coexist in immunosenescence: on the one hand, a decrease in the capacity of the immune response and, on the other hand autoantibody production. The possible consequences of this progressive 'ageing' of the immune system are the increase in autoimmune phenomena, incidence of neoplasia and predisposition to infections. The study of autoimmune manifestations in elderly populations should be considered a priority for future medical research because of increasing life expectancy, especially in developed countries. This review analyses the main immune disorders associated with immunosenescence, the prevalence and clinical significance of autoantibodies in the elderly and the clinical expression of the main autoimmune diseases in older patients.

Aged↗

PubMed2006

A case of polyglandular autoimmune syndrome type III complicated with autoimmune hepatitis.

A 58-year-old woman complaining of finger tremor was referred to our hospital. The diagnosis of Graves' disease was made based on increased free triiodothyronine (18.88 pg/ml) and free thyroxine (7.47 ng/dl), low TSH (<0.005 microIU/ml) and increased TSH receptor binding antibody activity (70.9%). Serum level of AST (62 U/l) and ALT (93 U/l) were increased and liver biopsy revealed linkage of adjacent portal areas by lymphoplasmacytic infiltrates and fibrosis with piecemeal necrosis. Although antinuclear antibody was negative, these findings indicated that she had autoimmune hepatitis (AIH) according to the criteria of the International Autoimmune Hepatitis Scoring System. Slowly progressive type 1 diabetes mellitus (DM) was confirmed by a diabetic response pattern due to 75 g-oral glucose tolerance test, and seropositivity towards anti-glutamic acid decarboxylase (725 U/ml) and islet cell (80 JDF Units) antibodies. This case exhibited an extremely rare combination of three different autoimmune diseases, including Graves' disease, slowly progressive type 1 DM and AIH, and had no known sensitive human leukocyte antigen (HLA) typing or haplotype for these disorders. Although it is common for patients with Graves' disease to exhibit abnormal liver function, it is important to make an accurate diagnosis of AIH because of this life-threatening disorder.

Adrenocorticotropic Hormone↗

PubMed2005

How can the innate immune system influence autoimmunity in type 1 diabetes and other autoimmune disorders?

The environment is important in determining the onset of autoimmune diseases such as type 1 diabetes. Genetic susceptibility factors interact with the environment to trigger and modulate a series of immune responses that ultimately lead to destruction of the insulin-producing beta cells of the pancreas. Although T lymphocytes are thought to play a major pathogenic role in the pathogenesis of diabetes, undoubtedly other components of the immune system also contribute to this process. How the environment may alter the course of disease is unknown, although viruses have been implicated in triggering and/or exacerbating the disease process. In this review, we will focus on how infection, particularly with viruses, may influence the onset of type 1 diabetes and other autoimmune diseases. Mechanisms such as molecular mimicry, bystander activation, and uncontrolled polyclonal activation of the immune system may contribute to the immune pathogenesis. We will also explore the interaction of the innate immune system with adaptive immune responses in predisposing individuals to the development of autoimmunity.

Animals↗

PubMed2000

Re-analysis of clinical features of 89 patients with autoimmune hepatitis using the revised scoring system proposed by the International Autoimmune Hepatitis Group.

OBJECTIVE: The diagnostic criteria of autoimmune hepatitis (AIH) were recently modified by the International Autoimmune Hepatitis Group. This study was performed to assess the impact of the revised scoring system on the diagnosis of AIH. PATIENTS AND METHODS: We re-analyzed the clinical features of 89 patients diagnosed as AIH in Nagasaki Prefecture, Japan, using the revised scoring system, and compared the scores and final diagnosis with our previously published results using the original system. RESULTS: Of the 89 patients with AIH, 40 (45%) were classified using the new system as "definite" AIH, 41 (46%) as "probable" AIH, and 8 (9%) patients were categorized as "others". Of these, 37 (42%), 35 (39%), and 4 (4%) patients who were classified as "definite", "probable", and "others" by the original system remained in the same category by the revised system, respectively. However, 3, 4, and 6 patients were re-categorized as "definite" from "probable", "others" from "probable", and "probable" from "definite", respectively. The difference in aggregate scores between the above two systems ranged from -5 to +2. The main contributing factors to the changes in aggregate AIH score were "other autoimmune disease(s)" and "interface hepatitis without lobular involvement and bridging necrosis on liver histology". However, the main contributing factors to the demotions from "definite" to "probable" and form "probable" to "others" were those related to the characteristics of biliary diseases, i.e., antimitochondrial antibody positive, biliary changes in liver histology, and alkaline phosphatase: aspartate aminotransferase ratio between 1.5 and 3.0. Moreover, two patients who had no histological evidence of AIH were both re-categorized as "others" from "probable" AIH. CONCLUSION: Our results indicated that the diagnosis, whether based on the revised or original system, was the same in the majority of AIH patients, but the revised scoring system excluded cases who had features suggestive of biliary diseases from "definite" AIH, and also confirmed that a diagnosis of "definite" AIH should not be made without liver histology.

Adult↗

PubMed1999

[Deafness as an autoimmune phenomenon in a female patient with ulcerative colitis and autoimmune hepatitis].

In the last years it was confirmed that deafness could occur as an autoimmune phenomenon in patients with ulcerative colitis. The object of the work is to demonstrate by means of retrospective analysis the occurrence of deafness in a female patient with ulcerative colitis, appearing in early childhood with underestimated clinical signs and confirmed after clinical manifestation of autoimmune hepatitis. The notion of deafness as an autoimmune phenomenon in ulcerous colitis could allow its timely treatment, restoration and preservation of hearing.

Adolescent↗

PubMed2004

[Simultaneous occurrence of autoimmune hepatitis type III and autoimmune thyroiditis type III (Graves disease)].

The case of simultaneous clinical manifestation of autoimmune hepatitis (AIH) and autoimmune thyroiditis was described. The authors presented diagnostic difficulties often related to AIH. The interdependence between the liver and thyroid gland function was emphasized. Correlative occurrence of different diseases of autoimmune origin in the same patients indicates a particular genetic predisposition.

Adult↗

PubMedDate not supplied

Autoimmune chronic liver disease as a model of human autoimmunity.

Although clonal deletion and clonal energy have been demonstrated in transgenic mice, the findings that autoreactive B or T cells are present in healthy subjects suggest that they are not the sole mechanisms of tolerance. As regards helper T lymphocytes, tolerance to self-antigens can arise by preventing class II MHC expression on non-lymphoid cells and autoantigen presentation to helper T cells initiating the autoimmune response. Autoimmune chronic active hepatitis (CAH) seems to be a good model of self-tolerance bypass. Hepatocytes are able to express class II molecules and can perform accessory cell functions with respect to T cell clones generated from lymphocytes infiltrating the liver in autoimmune CAH patients. The class II antigen expression on hepatocytes may be modulated by IFN-gamma released by infiltrating T lymphocytes; thus, the activated liver cells can present autoantigens to autoreactive T cell clones. On the other hand, these findings may occur only when the upregulation of IFN-gamma or other lymphokines permits the expression of rare class II antigens on hepatocytes capable of binding particular residues of a liver-autoantigen which are recognized by specific autoreactive T cell clones binding different residues on the same epitope.

Autoimmune Diseases↗

PubMed1990

Reversal of autoimmune encephalomyelitis by membranes presenting myelin basic protein-associated class II MHC molecule as an approach to immunotherapy of organ-specific autoimmune diseases.

Experimental autoimmune encephalomyelitis (EAE), a well-accepted experimental model for multiple sclerosis in humans, is a paralytic disease mediated by CD4+ T cells specific for myelin basic protein (MBP). Several approaches to immune-specific therapy of EAE as a model for other organ-specific autoimmune diseases have previously been reported. We now show that macrophages (M phi) or B cells, as antigen-presenting cells, when pulsed with MBP and intraperitoneally (but not intravenously) inoculated after the encephalitogenic challenge, are highly effective in blocking the development of EAE. Moreover, M phi pulsed with an organ tissue homogenate, mouse spinal cord homogenate, can also present the relevant target antigen, MBP, and are as effective as MBP-pulsed M phi in blocking the development of EAE. This capacity of the M phi to identify and present the relevant target antigen indicates that this approach is also applicable to organ-specific autoimmune diseases other than EAE, regardless of how much is known about their etiological agent or specific target antigen. Nonviable glutaraldehyde-fixed MBP-pulsed M phi or membranes derived from MBP-pulsed M phi retain their capacity to block the development of EAE.

Animals↗

PubMed1996

5-azacytidine treatment induces autoimmune vitiligo in parental control strains of the Smyth line chicken model for autoimmune vitiligo.

The effect of 5-Azacytidine (5-AzaC) on melanization was examined in two sublines of the Smyth line (SL) chicken model for autoimmune vitiligo, in two MHC-matched vitiligo-susceptible but normally pigmented controls (BL), and in nonsusceptible controls (LBL). 5-AzaC was administered ip every 3 days from day of hatch to 18 weeks at levels of 1 or 3 mg/kg body wt. Both treatments increased (P < 0.01) the incidence of autoimmune vitiligo in BL controls. In contrast, treatment significantly depressed (P < 0.01) the expected high incidence of vitiligo in one SL subline, but not in the other. There were no apparent pigmentation changes in 5-AzaC-treated LBL controls. 5-AzaC had dose-dependent depressing effects (P < 0.01) on body and lymphoid organ weights. Histological and mitogen assay data suggest negative effects on lymphocyte number and function. The data show that 5-AzaC can initiate autoimmune disease in genetically susceptible but phenotypically normal individuals.

Animals↗

PubMed1998

The association of MHC with autoimmune diseases: understanding the pathogenesis of autoimmune diabetes.

The current paradigm of MHC and disease association is efficient binding of autoantigens by disease-associated MHC molecules leading to a T cell-mediated immune response and resultant autoimmune sequelae. Data presented here offer a different model for this association of MHC with autoimmune diabetes. This new explanation suggests that the association of MHC with autoimmunity results from "altered" thymic selection in which high-affinity self-reactive (potentially autoreactive) T cells escape negative selection. This model offers an explanation for the requirement of homozygous MHC class II expression in NOD mice (and in man) in susceptibility to IDDM.

Animals↗

PubMed2005

Autoimmune gastritis is a well-defined autoimmune disease model for the study of CD4+CD25+ T cell-mediated suppression.

Autoimmune gastritis (AIG) is an experimental model that closely resembles human autoimmune gastritis, the underlying pathology of pernicious anemia. Pathogenic CD4+ T cells are reactive to the parietal cell autoantigen, H/K ATPase, and are controlled by CD4+CD25+ T cells in an immunosuppressive cytokine-independent manner. Comparison of CD4+CD25+ T cell-mediated suppression in other autoimmune models shows inconsistencies with respect to requirements of cytokines for immunosuppression. More recent data, however, indicate that the evidence for requirement of IL-10 and TGF-beta could be due to the complex nature of the T cells causing the disease as well as the role of induced regulatory T cell populations. AIG provides a well-defined model that may allow for better analysis of CD4+CD25+ T cell in vivo biology. Evidence from this model indicates that immune responses must be initiated and then CD4+CD25+ T cells are recruited to control the quality of the immune response.

Anemia, Pernicious↗

PubMed1980

Spontaneous autoimmune reactions against pancreatic islets in mouse strains with generalized autoimmune disease.

The spontaneously autoimmune mouse strains NZB, NZB X NZW, MRL and BXSB have been examined for signs of autoimmune reactions against islet cells. Between 15 and 55 animals of each strain were tested. Infiltrates of lymphocytes and fibroblasts into pancreatic islets were found in more than 80% of NZB mice, in about 50% of MRL and NZB X NZW mice, and in less than 20% of BXSB mice. Infiltrates were not found in the exocrine portion of pancrea. All NZB mice had abnormal glucose tolerance. In the three other strains between 20 and 50% of animals had abnormal glucose tolerance. All mice had fasting normoglycaemia. The lesions in NZB mice were studied in more detail. It was found by ultrastructural analysis that in young mice pancreatic infiltrates consisted of lymphocytes and fibroblasts. Single lymphocytes were also seen outside the main infiltration area. After 2 to 5 months of age another type of infiltrate, consisting of lymphocytes and macrophages was observed. B-cell destruction by lymphocytes was apparent in both young and adult NZB mice. It is concluded that cellular autoimmune reactions against pancreatic islets may occur spontaneously as a consequence of immunological disorders in NZB, NZB X NZW and MRL mice.

Animals↗

PubMed1993

Abnormal sympathetic skin response in patients with autoimmune vitiligo and primary autoimmune hypothyroidism.

The sympathetic skin response was studied in 21 patients with autoimmune vitiligo or hypothyroidism or both. No response to stimulation was found in 6 patients, but 4 with both diseases showed abnormal results. Sympathetic skin response is useful in evaluating sudomotor activity of the autonomic nervous system, and it is concluded that patients with autoimmune vitiligo, autoimmune hypothyroidism and especially those with both diseases show evidence of sudomotor dysfunction.

Autoimmune Diseases↗