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PubMed1990

Development of antigen-specific therapies for autoimmune disease.

Reversal of autoimmune disease with monoclonal antibodies to polymorphic determinants associated with class II gene products of the major histocompatibility complex (MHC) and to T-cell receptor variable region segments has been demonstrated in animal models. Recent studies have shown that it is also possible to use mutant peptides to block recognition of self-antigen associated with MHC by T-cells that mediate autoimmune disease. These mutant peptides have been used to prevent the model autoimmune condition experimental allergic encephalomyelitis. The possibility of extending these approaches to human disease is discussed.

Amino Acid Sequence↗
PubMed1990

Could specific oral tolerance be a therapy for autoimmune disease?

Several experimental autoimmune diseases have been successfully suppressed by the induction of specific oral tolerance. Here, Stephen Thompson and Norman Staines review the nature and mechanisms of this form of tolerance and discuss its possible applications in the control of human autoimmune diseases.

Administration, Oral↗
PubMed1998

Cardiovascular manifestations of systemic autoimmune diseases.

The systemic autoimmune diseases are a protean group of illnesses that primarily affect the joints, muscles, and connective tissue. All aspects of the cardiovascular system can be involved with clinical consequences ranging from asymptomatic abnormalities to serious life-threatening conditions. This article discusses the cardiovascular manifestations of the systemic autoimmune diseases with particular focus on clinical pathophysiology and management.

Autoimmune Diseases↗
PubMed1995

Antibodies to human immunodeficiency virus (HIV-1) in autoimmune diseases: primary Sjögren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and autoimmune thyroid diseases.

The aetiology of autoimmune diseases remains unknown. The relationship between virus, and more recently retrovirus, has been suggested with this group of diseases. Immunoblotting is a useful method for determining the presence of proteins coded by different retrovirus genes. Since the prevalence of these types of proteins in patients with primary Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and autoimmune thyroid diseases has not been fully established, the aim of this work was to determine the prevalence of antibodies to immunodeficiency human virus type 1 (HIV-1) proteins in these diseases and their possible relationship with the presence of anti-nuclear, anti-DNA, anti-SSA (Ro) and anti-SSB (La) autoantibodies. Antibodies to human immunodeficiency virus (HIV-1) were studied in a group of 341 patients with autoimmune diseases (77 SS, 98 SLE, 75 RA, 91 autoimmune thyroid diseases) and 126 blood donors as a control group. A Western blot was used to detect antibodies to HIV-1, and a double polymerase chain reaction (PCR) using nested primers in the gag and pol gene of HIV-1. Antinuclear antibodies, anti-DNA, anti-SSA (Ro) and anti-SSB (La) were determined by enzyme-linked immunosorbent assays. At least one band was shown on immunoblotting in 26% of patients with autoimmune diseases and 35% of controls. The presence of antibodies to p55 or p68 proteins in patients with SS or SLE proved to be the only statistically significant difference between the other autoimmune diseases studied and the control group. These antibodies were not associated with autoantibodies ANA, DNA, SSA (Ro) or SSB (La).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Experimental autoimmune gastritis: mouse models of human organ-specific autoimmune disease.

Experimental autoimmune gastritis (EAG) is an excellent model of human autoimmune gastritis, the underlying cause of pernicious anaemia. Murine autoimmune gastritis replicates human gastritis in being characterized by a chronic inflammatory mononuclear cell infiltrate in the gastric mucosa, destruction of parietal and zymogenic cells, and autoantibodies to the alpha-and beta-subunits of the gastric H+/K+ ATPase. Disease is induced strain specifically in gastritis-susceptible BALB/c mice by methods with a greater variety than those for most other experimental autoimmune diseases. The disease is induced in the regional gastric lymph node in which pathogenic CD4+ T cells are recruited. The model provides an excellent illustration of regulation by CD4+CD25+T cells, and, indeed, the removal of such regulatory cells, e.g., by neonatal thymectomy, is thought to be a major mechanism by which disease can develop. The culprit T helper type 1 (Th1) CD4+ T cells recognize either the alpha- or beta-subunits of the gastric H+/K+ ATPase, but the beta-subunit appears to be the initiating autoantigen, while the alpha-subunit may have a role in perpetuating disease. Since no specific environmental modifiers are identifiable, the origins of the disease are intrinsic; this is illustrated by the capacity of a cytokine (GM-CSF)-dependent inflammatory stimulus in the stomach to initiate EAG, according to a transgenic model in which thymectomy is dispensible. Thus, EAG is an exquisite model for a reductionist analysis of the multiple elements that in combination induce autoimmunity in humans.

Anemia, Pernicious↗
PubMedDate not supplied

Idiotypic network dysregulation: a common etiopathogenesis of diverse autoimmune diseases.

The pathogenesis of autoimmune disease is still an enigma. Whereas the diverse clinical manifestations of many autoimmune diseases cannot be explained by the existence of autoantibodies, idiotypic dysregulation may provide an alternative explanation. Experimental models, serum level changes of pathogenic idiotypes during exacerbation and remission, and the increased expression of pathogenic idiotypes following common infections all support this notion. In this article we review experimental models of autoimmune disease induction (systemic lupus erythematosus, antiphospholipid syndrome, Goodpasture's syndrome, autoimmune thyroiditis, and vasculitis) by manipulation of the idiotypic network, and discuss the utilization of idiotypes for the immunotherapy of autoimmune diseases and other conditions that involve the immune system (e.g., atherosclerosis).

Animals↗
PubMed1996

[Malignancy in autoimmune diseases].

Association between antecedent autoimmune diseases and malignancy, including lympho-proliferative disorders (LPD), has been reported in generalized autoimmune diseases such as systemic lupus erythematosus (SLE), dermatomyositis (DM) and rheumatoid arthritis (RA), and also in organ-specific autoimmune diseases such as Sjögren's syndrome (SS) and chronic thyroiditis. In this paper, LPD were summarized for DM, SLE, RA and SS, and some etiologic factors were considered. In surveying previous Japanese literature on the topic, it was revealed that LPD occur frequently in DM similar to various types of cancer. The period between the occurrence of cancer and DM is usually within 12 months, suggesting that the etiologic factor may differ between cancer and LPD in DM. Sixty one cases (20.0%) of monoclonal non-malignant LPD were observed among our 306 patients with SS. Fifteen cases (5.0%) of malignant LPD such as malignant lymphomas (13 cases) and Waldenström's macroglobulinemias (2 cases) were also seen among our SS patients. The activation of rheumatoid factor genes such as Humkv 325 and Vg was considered as one of the triggering factors to advance LPD from the benign to malignant state. A high amount of the bcl-2 protein expression was detected in lymphoepithelial lesions of salivary glands in patients with SS, suggesting that the activation of this gene plays an important role in the progression of the lesion from benign to malignant LPD. Accumulation of many genetic abnormalities including bcl-2 and p 53 genes by chronic stimulation of T and B cells at the site of the autoimmune reaction may be important in the high occurrence of LPD in patients with autoimmune diseases.

Autoimmune Diseases↗
PubMed2005

Cardiac imaging techniques in systemic autoimmune diseases.

Systemic autoimmune disorders are frequently associated to cardiac involvement and to a high prevalence of ischemic coronary events, often occurring at a younger age than in the normal population. Large increase in mortality is related to premature atherosclerosis with coronary artery disease and stroke in patients with connective tissue diseases. Coronary heart disease is responsible for 40-50% of the deaths of patients with rheumatoid arthritis. Transesophageal or transthoracic echocardiography are the most useful and noninvasive techniques able to detect not only valvular abnormalities, embolic sources or pulmonary hypertension, but also left ventricular systolic or diastolic dysfunction. Furthermore, the introduction of new indexes, contrast agents and software increased the accuracy of this technique. It is possible now to evaluate coronary flow reserve by transthoracic echocardiography in patients with systemic autoimmune disease in order to detect microvasculature disorder. However, an ischemic response in a symptomatic patient requires, in most cases, further evaluation with cardiac catheterization. Coronary artery imaging allows confirmation of the presence, extent and position of atheromatous lesions. More recently, other imaging modalities including magnetic resonance and computerized tomography angiography have been developed to allow imaging of the coronary arteries.

Autoimmune Diseases↗
PubMed2003

Potential use of drugs that target neural-immune pathways in the treatment of rheumatoid arthritis and other autoimmune diseases.

Many autoimmune disorders share two common features, dysregulation of the immune system and stress pathways. Two stress pathways, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS), regulate immune system responses, through release of corticosteroids and norepinephrine (NE), respectively. These neuromediators act on immune cells via specific receptors on their surface to modulate the production of key regulatory cytokines. Glucocorticoids modulate immune responses by glucocorticoid binding to cytoplasmic glucocorticoid receptors within target cells. NE regulates immune responses through interaction with plasma membrane beta- or alpha-adrenergic receptors (AR). Both NE and glucocorticoids promote humoral immunity by altering macrophages and T cell cytokine production after an antigen challenge. Glucocorticoids and NE do this by inhibiting interleukin (IL)-12, and interferon (IFN)-gamma, which drives cell-mediated immunity. Additionally, catecholamines drive humoral immunity by stimulating macrophage IL-10 production. These catecholamine effects are mediated largely via beta(2)-AR activation. Both glucocorticoids and NE inhibit inflammation. However, under some circumstances NE promotes inflammation through interaction with macrophage alpha1-AR and subsequent increases in tumor necrosis factor alpha (TNFalpha production. Although macrophages do not normally express alpha(1)-AR, expression of this receptor on macrophages and monocytes occurs in some disease states, including rheumatoid arthritis (RA). Through these mechanisms the HPA axis and the SNS influence the course and progression of RA. Thus, the HPA axis and the SNS are likely to play key roles in the pathology of RA. Furthermore, therapeutic agents targeting the neural pathways that normally regulate immune system homeostasis may prove beneficial for treating RA and other autoimmune diseases.

Adjuvants, Immunologic↗
PubMed1990

Human adjuvant disease: remission of silicone induced autoimmune disease after explanation of breast augmentation.

Autoimmune diseases following silicone or paraffin implantation are rarely encountered complications of plastic surgery. A 42 year old woman is presented who developed clinical and immunological features of systemic lupus erythematosus 11 years after silicone augmentation. After explanation antinuclear antibody titres decreased from 1/1280 to 1/160, C4 complement fraction and the previously raised angiotensin converting enzyme normalised in step with clinical improvement. It is important that plastic surgeons and rheumatologists should be aware of this possible association.

Adult↗
PubMed2002

Animal models of endocrine/organ-specific autoimmune diseases: do they really help us to understand human autoimmunity?

Organ-specific or endocrine autoimmune diseases are complex, polygenic afflictions the penetrance of which is heavily dependent on various environmental influences. Important target tissues are the thyroid, the islets of Langerhans, gastric parietal cells and steroid-producing cells in the adrenal and ovary. The etiology of these diseases remains to be clarified. The pathogenesis is strongly associated with autoimmune phenomena. None of the current treatment approaches provides a cure; rather they represent replacement therapy. An important objective in the treatment of endocrine/organ-specific autoimmune diseases is the detection of individuals at risk for the development of such diseases and the development of interventions to prevent an outbreak of the diseases. This requires an exquisite knowledge of the early etio-pathogenic stages of these diseases. This review concentrates on the usefulness of animal models for a precise understanding of these very early stages. It must be emphasized that studying animal models cannot answer all the problems presented by endocrine/organ-specific autoimmune diseases as seen in the clinic. It must be expected - considering the different etiologies in the different animal models (see below) - that the causes of the diseases in the human and the involvement of various genes and environmental factors may also vary. Yet, particularly in the study of the pre-autoimmune phases of the diseases, there is hardly any alternative to the study of animal models. Only limited series of experiments can be carried out in human subjects at risk to develop such diseases. Moreover, a general semblance (blueprint) of the etio-pathogenesis found in the animal models can lead the way for human studies. Efforts to understand the patho-physiology of the early stages of endocrine/organ-specific autoimmune diseases have mainly involved animal models that "spontaneously" develop such diseases. Of these the bio-breeding diabetes-prone (BB-DP) rat and the non-obese diabetes (NOD) mouse are the most well studied, yet many studies have also been carried out in the obese strain (OS) chicken. Apart from these spontaneous models there are animal models that are induced by environmental perturbations (viruses, toxic substances), by thymectomy procedures or by genetic manipulations, e.g., the RIP-LCMV model and the BDC 2.5 TCR mouse model. A general blueprint has emerged from the studies into the early stages of the pathogenesis of endocrine/organ-specific autoimmune diseases in these animal models: animals at risk to develop endocrine/organ-specific autoimmune diseases show various pre-autoimmune aberrancies in their target glands, T cells, macrophages (Mphi) and dendritic cells (DC). The presumably aberrant target cells, T cells, DC and Mphi need to interact abnormally before autoimmune disease can fully develop. In this abnormal interaction additional aberrancies in other regulatory systems may play a role in a further exacerbation of the self-directed immune response, such as defects in the hypothalamus pituitary adrenal (HPA) axis system. The various aberrancies are partly genetically determined by a variety of separate genes, particularly MHC-related genes, but they may also be environmentally induced (e.g., via viruses, high iodine diet, and other experimental manipulations). Recently evidence has been gathered for pre-autoimmune aberrancies similar to the animal models in the DC/ Mphi compartment and the HPA axis in humans at risk to develop endocrine/organ-specific autoimmune diseases. However, analogous pre-autoimmune abnormalities in human target glands or in T cell function have not yet been found with certainty. We believe that animal models of endocrine/organ-specific autoimmune disease still hold immense promise for the discovery of pathways, genes and environmental factors that determine the development of endocrine/organ-specific autoimmune diseases. Animals affected by such diseases provide a unique opportunity to uncover disease-associated pathways, which are complicated to define in man.

Animals↗
PubMed2000

[Autoimmune diseases].

In most autoimmune diseases no specific cause can be identified. Autoimmune disorders are induced by a loss of tolerance where self cannot be differentiated from foreign. Infections can provoke autoimmune processes, e.g. rheumatic fever. The degree of severity and the extent of disease are influenced by environmental factors and genetic characteristics. The identification of antibodies can be helpful for diagnosis. Certain antibodies are associated with specific manifestations (e.g. Ro-antibodies). Often, however, antibodies are nonspecific. Despite considerable progress in treatment, cure is rare. Treatment of autoimmune diseases requires continuous consideration of clinical activity and necessity of medication.

Autoimmune Diseases↗
PubMed1989

Dermatological autoimmune diseases and the multiple autoimmune syndromes.

The association of autoimmune pathologies with cutaneous diseases has received little attention, except for their association by twos. The combination of at least three autoimmune diseases in a same patient has recently been defined as a Multiple Autoimmune Syndrome (MAS). The purpose of this article is to define the place of dermatological autoimmune conditions (vitiligo, alopecia areata, pemphigus, bullous pemphigoid, dermatitis herpetiformis) among the MAS and to stress the clinical aspects that may aid dermatologists in the care of their patients.

Autoimmune Diseases↗
PubMed2006

Endometriosis associated with defective handling of apoptotic cells in the female genital tract is a major cause of autoimmune disease in women.

Several autoimmune diseases are far more common in women than men. The reasons are unknown. Recent studies have shown that many autoimmune diseases which predominantly affect females are characterized by the production of autoantibodies against components of apoptotic cells. Furthermore, in experimental animals, defective clearance of apoptotic cells in a pro-oxidant inflammatory environment can trigger the production of these autoantibodies and related autoimmune disease. Endometriosis is characterized by defective clearance of apoptotic endometrial cells in a pro-oxidant inflammatory environment. It is proposed that this combination of abnormalities triggers autoantibody production in women affected by endometriosis. A proportion of these women will be genetically predisposed to develop overt autoimmune disease. As endometriosis affects at least 4% of the female population of reproductive age, this phenomenon will have a major effect on the gender prevalence of several related autoimmune syndromes. The hypothesis is supported by epidemiological studies which show a strong association between endometriosis and female-predominant autoimmune disorders.

Apoptosis↗
PubMed1997

Infertility in women with pemphigus vulgaris and other autoimmune diseases.

BACKGROUND: Pemphigus vulgaris (PV) is an autoimmune disease. Autoimmune diseases may adversely affect reproductive function and could result in infertility. OBJECTIVE: Our purpose was to describe nine young women with PV and infertility. METHODS: A retrospective study was performed. Clinical characteristics, immunopathologic features, treatment, clinical course, and long-term follow-up were determined. RESULTS: Eight of nine patients were unable to become pregnant. One patient became pregnant during a period of remission. In eight of the nine patients, the cause of infertility was ovarian. Anti-sperm antibodies were present in two of the patients. CONCLUSION: Some patients with PV may have infertility. No definitive conclusion about the frequency of infertility in these patients or its relation to PV can be drawn. However, these observations indirectly demonstrate that there may be important interactions between the immune and hormonal systems.

Adult↗
PubMed2005

Bovine spongiform encephalopathy, multiple sclerosis, and creutzfeldt-jakob disease are probably autoimmune diseases evoked by Acinetobacter bacteria.

Bovine spongiform encephalopathy (BSE) belongs to a group of conditions named together as transmissible spongiform encephalopathies (TSE). They are fatal neurodegenerative diseases that include "scrapie" in sheep, Creutzfeldt-Jakob disease (CJD) and kuru in humans, and chronic wasting disease in deers. BSE-affected animals suffer from "hindquarters" paralysis, which is also one of the main features of "experimental allergic encephalomyelitis" (EAE). EAE is considered an animal model of multiple sclerosis (MS) and lower limb ataxia is often observed in MS patients. The presence of clinical and histopathological similarities in these diseases suggests a common pathology. Specific brain peptides, which produce EAE, were shown to have "molecular mimicry" with the soil and skin saprophytic microbe, Acinetobacter. BSE-affected animals and patients suffering from MS have been found to have elevated levels of antibodies to both Acinetobacter and Pseudomonas bacteria, as well as autoantibodies to both white and gray matter brain components. The hypothesis is proposed that Acinetobacter/Pseudomonas bacteria may have evoked both BSE and MS through the mechanism of "molecular mimicry" and autoimmunity in a similar way to Streptococcus microbes producing rheumatic fever and Sydenham's chorea. The possibility that CJD patients may show similar features remains to be determined.

Acinetobacter↗
PubMed1997

Epidemiology and estimated population burden of selected autoimmune diseases in the United States.

Autoimmune diseases cause significant and chronic morbidity and disability. The actual number of persons in the United States that are affected by autoimmune diseases and the resultant magnitude of their impact on the public's health are limited to a few specific diseases. In order to understand the clinical, public health and economic importance of these diseases it is necessary to have estimates of incidence and prevalence rates in the population. In this analysis, we estimate the number of persons affected by 24 autoimmune diseases in the United States by applying mean weighted prevalence and incidence rates obtained from published articles to U. S. Census data. The study was restricted to 24 autoimmune predefined diseases for which there was direct or indirect evidence for autoimmune pathogenesis. Subsequently, we used computerized search software and ancestry searching (bibliographies) to conduct a comprehensive search of articles published from 1965 to the present. Eligible studies included those which adhered to standard disease definitions and which included population-based estimates of incidence or prevalence rates. Mean weighted incidence and prevalence rates were calculated from eligible published studies with greater weight proportionately given to larger studies. The mean rates were then applied to the U.S. Census population figures to estimate the number of persons currently afflicted with each disease and the number of new cases occurring each year in the United States. Only U.S. and European studies were used to estimate prevalence and incidence rates when there were at least six eligible studies available for a disease. When there were fewer than six studies, all available studies were included, regardless of country of origin. The number of eligible incidence and prevalence studies found in the literature varied considerably between the 24 autoimmune diseases selected. The largest number of eligible prevalence studies were conducted on multiple sclerosis (MS), rheumatoid arthritis, and systemic lupus erythematosus (SLE) (>/=23), followed by insulin-dependent diabetes (IDDM), myasthenia gravis, primary biliary cirrhosis, and scleroderma (>/=7). There were only one to four eligible studies done on 11 other diseases, and no prevalence studies on 6 diseases. Incidence studies were less frequent but the largest number of studies were conducted on IDDM (n = 37) and MS (n = 28), followed by Graves' disease/hyperthyroidism, glomerulonephritis, primary biliary cirrhosis, rheumatic fever, rheumatoid arthritis, scleroderma, and SLE (>/=9). On the other 11 diseases, there were one to six eligible studies, and no studies on 5 diseases. There were no eligible incidence or prevalence studies on Goodpasture's syndrome, idiopathic thrombocytopenia purpura, or relapsing polychondritis. Overall we estimate that 8,511,845 persons in the United States or approximately 1 in 31 Americans are currently afflicted with one of these autoimmune diseases. The diseases with the highest prevalence rates were Graves'/hyperthyroidism, IDDM, pernicious anemia, rheumatoid arthritis, thyroiditis, and vitiligo, comprising an estimated 7,939, 280 people or 93% of the total number estimated. Glomerulonephritis, MS, and SLE added an estimated 323,232 people. The prevalence of the other diseases reviewed were rare, less than 5.14/100,000. Most diseases were more common in women. From the incidence data we estimate that 237,203 Americans will develop an autoimmune disease in 1996 and that approximately 1,186,015 new cases of these autoimmune diseases occur in the United States every 5 years. Women were at 2.7 times greater risk than men to acquire an autoimmune disease. After reviewing the medical literature for incidence and prevalence rates of 24 autoimmune diseases, we conclude that many autoimmune diseases are infrequently studied by epidemiologists. As a result the total burden of disease may be an underestimate. (ABSTRACT TRUNCATED)

Autoimmune Diseases↗