Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis and etiology of the ophthalmopathy associated with Graves' disease still remains to be elucidated. There is, however, general consensus that the extraocular muscles are the principal site of the autoimmune response and that the main changes are in the interstitium. The primary target seems to be the fibroblasts which are stimulated as a result of cytokine release by the activated T-cells that accumulate in the muscles. Increased production of glycosaminoglycans and collagen by fibroblasts, attracts water to the interstitium and produces interstitial oedema. The frequent association of Graves' thyroid disease and ophthalmopathy favours the hypothesis of antibodies cross-reacting with antigens of orbit and thyroid. Although cross-reactivity is very attractive, the nature of the involved antigen remains unknown. Since Graves' ophthalmopathy is an autoimmune disorder, many immunomodulatory agents have been used in the treatment of this disorder. Anti-inflammatory and immunosuppressive treatment modalities will be reviewed.
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PMID:Pathogenesis and treatment of the ophthalmopathy associated with Graves' disease. 134 54

Increased knowledge of the etiopathogenesis of Type 1 diabetes has focused great interest on the possibilities of preventing the disease. Type 1 diabetes is considered to be a chronic autoimmune disease characterized by gradual beta-cell destruction mediated by autoreactive T-lymphocytes during an asymptomatic prediabetic phase of varying duration. Both experimental and epidemiologic data indicate that nutritional cow milk exposure early in life may play a critical role in the initiation of beta-cell destruction. Accordingly a primary prevention study has been planned to test the hypothesis that dietary elimination of cow milk proteins over the first 9 months of life will decrease the subsequent risk of childhood type 1 diabetes in high risk infants. The possibility of identifying prediabetic individuals before decisive loss of beta-cell function by various islet cell-specific autoantibodies enables measures of secondary prevention in the prediabetic phase. There are indications from experimental and human studies that nicotinamide, a water-soluble group B vitamin, may be effective in preventing or delaying the presentation of diabetes. A European multicentre study will be initiated in the near future to explore whether oral nicotinamide can prevent or delay the clinical manifestation of Type 1 diabetes in high risk first degree relatives of diabetic children. We have to wait for the results of these intervention studies for years, and similarly other prevention strategies have to be tested in large-scale long-lasting clinical trials. Nevertheless, prevention of childhood diabetes may become a reality in the next century.
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PMID:[Can type-1 diabetes in children be prevented?]. 140 25

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease. It is widely used as an animal model of multiple sclerosis (MS). We studied the prophylactic effects of FK 506 electrophysiologically and immunohistochemically in acute EAE. Female Lewis rats were sensitized with guinea pig spinal cord in complete Freund's adjuvant. FK 506 suspended in distilled water was orally administered at 1.0, 3.2, 5.0 or 10.0 mg/kg per day for 12 successive days starting from the day of sensitization. A placebo was used as the control. Administration of FK 506 at doses of 3.2 mg/kg per day and over significantly delayed the onset of clinical signs. However, the FK 506 group showed a relapse or a chronic state following the onset of EAE. We made a time course recording of cortical somatosensory evoked potential (cortical SEP: P 15). P 15 latency in the placebo group was significantly delayed in accordance with the clinical signs and showed immediate improvement upon recovery. Prolongation of P 15 latency in the FK 506 group also occurred concomitantly with the clinical signs, but the delay continued after the loss of symptoms as well. After the onset of EAE, the infiltrating lymphocyte subset was examined by the avidin-biotin peroxidase complex (ABC) method in the lumbar spinal cord. In the placebo group, the number of OX3+ (Ia) cells and the W 3 25+: OX8+ (helper/inducer T: suppressor/cytotoxic T) ratio clearly reflected the development and remission of EAE. In the FK 506 group, however, increases in OX8+ lymphocytes were observed irrespective of clinical sign fluctuation, and there were corresponding decreases in the W 3/25+: OX8+ ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of novel immunosuppressant FK 506 in acute experimental allergic encephalomyelitis]. 169 82

NZB and BXSB mice develop autoimmune disease and learn poorly on avoidance tasks. In addition, many of these mice have ectopic collections of neurons, which occur prenatally, in layer I of the cerebral neocortex. The purpose of these experiments was to evaluate the contribution of the uterine/maternal environment upon these variables by transferring fertilized ova to an autoimmune or a non-autoimmune maternal host. In Experiment 1 fertilized DBA ova were transferred into the uteri of BXSB maternal recipients. Later, these animals and conventionally reared DBAs were tested for paw preference, swimming rotation, water escape learning, and shuttlebox avoidance learning. Blood was taken for measurement of immune parameters, and their brains were examined for cortical ectopias. As compared to conventional DBAs, the ova transfer mice had greater amounts of anti-dsDNA autoantibodies, poorer avoidance learning, and poorer water escape learning; in addition, the females had greater paw asymmetry. There was only 1 ectopia in the 81 ova transfer animals, and none in the 78 control mice. In Experiment 2 fertilized NZB ova were transferred into the uteri of non-autoimmune hybrid females and the same procedures were followed as in Experiment 1. Ova transfer mice had lesser amounts of anti-dsDNA autoantibodies, better avoidance learning scores, and females had less paw asymmetry; in addition, within the ova transfer group males were clockwise swimmers whereas females swam counterclockwise. There were 4 ectopics out of 17 ova transfer mice (23.5%), which did not differ from the 40.5% of the control group. In both experiments the uterine environment did not affect the occurrence of ectopias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of the autoimmune uterine/maternal environment upon cortical ectopias, behavior and autoimmunity. 178 24

NZB and BXSB mice were given a battery of behavioral tests including paw preference, water escape, Lashley III maze, and discrimination learning. Their brains were then evaluated for cortical ectopias. The incidence of ectopias was 40.5% in NZBs and 48.5% in BXSBs. In the NZB strain left-pawed ectopic mice (both male and female) had the fastest swimming time in the water escape test, while right-pawed ectopics were the slowest. The same findings were obtained for left- and right-pawed ectopic BXSB males, but not for the females. However, on discrimination learning the BXSB males had the exact opposite pattern: right-pawed ectopics were the best learners while left-pawed ectopics were the worst. Male BXSBs and both male and female NZBs were manifesting autoimmune disease at the time of testing, while female BXSBs were not, suggesting that autoimmunity is a necessary background condition for the differential expression of ectopias and paw preference upon learning processes. The finding that the left-pawed ectopic BXSB mice, who were the poorest learners in the non-spatial discrimination learning test, learned best in the spatial water escape test is in agreement with the Geschwind hypothesis that pathological events during brain development may, in some instances, produce superiority of function.
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PMID:Spatial learning, discrimination learning, paw preference and neocortical ectopias in two autoimmune strains of mice. 179 76

It is well established that insulin-dependent diabetes (IDDM) is an autoimmune disease with a strong genetic link to the HLA locus. It is less well understood, however, how the destruction of the insulin-producing beta cells is effected and why neighboring non-beta islet cells are spared. Also incompletely explained are the observations that, unlike other autoimmune diseases such as multiple sclerosis, IDDM does not preferentially affect females, the incidence of the disease is highest among young adults, and there are temporal correlations between the onset of the disease and emotional trauma. We have addressed some of these questions by using transgenic mice that constitutively express the MHC class I antigen Dd in the beta cells of the pancreas. Although both male and female Ins.Dd mice expressed equivalent amounts of the Dd protein only the males developed diabetes. The diabetes in the males could be reversed by castration, and the normoglycemic females became diabetic following either ovariectomy and the implantation of a slow-release pellet containing testosterone or the inclusion of dexamethasone in the drinking water. In contrast, transgenic mice that expressed the herpes simplex virus type 1 glycoprotein D in the pancreatic beta cells were normoglycemic and showed no obvious histopathological consequences. The observation that the beta-cell dysfunction by the increased expression of the MHC class I protein Dd cannot be induced by the herpes viral protein suggests that the cellular damage is related to a specific structure or function of the MHC proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Male-specific beta-cell dysfunction and diabetes resulting from increased expression of a syngeneic MHC class I protein in the pancreata of transgenic mice. 196 48

Primary Sjogren's syndrome (SS) is an autoimmune disorder primarily affecting salivary and lacrimal glands. Durational measures of the oral phase of swallowing were obtained on 34 patients with primary SS and 34 age-matched controls from analyses of ultrasound scans. Two conditions were examined: a basal (BA) swallow (only endogeneous secretions present in the subjects' mouths) and a 10 ml water bolus (WB) swallow. The patients with SS produced swallowing durations significantly longer (p less than 0.05) than those of the controls for each of the two conditions. Moreover, unlike normals, over 40% of the patients with SS produced WB swallows that were longer than their BA swallows. For further analyses, patients with SS were classified into two groups based on the difference in duration between their BA and WB swallows. These two groups differed from each other on clinical evaluations of oral motor function and presenting complaints. No significant differences were found between these two groups for salivary function or immunologic profile. These findings support the hypothesis that dysphagia can result from conditions leading to salivary gland dysfunction and document the need for the assessment of swallowing function in patients with Sjogren's syndrome.
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PMID:Objective measures of swallowing in patients with primary Sjogren's syndrome. 270 Oct 92

One hundred patients with ischemic finger ulceration had detailed prospective evaluation to determine the incidence of associated diseases, response to treatment, and natural history of the condition. A potentially serious associated disease was detected in each patient including autoimmune disease in 54%, Buerger's disease in 9%, arteriosclerosis obliterans in 9%, hypersensitivity angiitis in 22%, and miscellaneous diseases in 6%. Conservative treatment with soap and water scrubs, antibiotics, and local resection/debridement resulted in long-term healing without recurrence in 88% of patients. Most recurrences occurred in patients with autoimmune disease, usually scleroderma or CRST.
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PMID:Upper extremity ischemia caused by small artery disease. 366 61

NZB mice have previously been shown to be deficient in the production of interleukins 1 and 2 (IL-1, IL-2) during the development of autoimmune disease. One or both of these defects have been inherited in certain of the NZB X C58 recombinant inbred strains (N X 8 RI). Certain of these strains have been selected to examine further the effect of decreased production of IL-1 and/or IL-2. The interleukin deficiencies found in vitro were not due to the presence of an inhibitor/suppressor nor was any activity found intracellularly upon water lysis of stimulated cells. Despite profound IL-1 and/or IL-2 deficiencies measured in vitro, all of the N X 8 RI lines examined were found to be capable of producing IL-1 in vivo as shown by their serum amyloid A response to endotoxin injection. We conclude from these studies that defects in IL-1 production measured in vitro do not reflect inability to produce this lymphokine in vivo. Young, IL-1 deficient NZB mice generated CTL to TNP-self but old, IL-2 deficient NZB mice did not. Since all other strains were found to generate cytotoxic T cells to TNP-self regardless of interleukin defects, we also conclude that the cytotoxic T cell defect in NZB mice is due to some presently unknown factor in addition to IL-2 deficiency. The relationship of decreased production of interleukins to the development of autoimmunity remains undefined.
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PMID:Functional consequences of perceived interleukin deficiencies? Analysis employing NZB x C58 recombinant inbred mice. 387 52

Hypothyroidism is commonly thought to cause decreased gastric emptying and secretion, but these may be related to associated autoimmune disease or chronic changes. Therefore, we measured gastric emptying and secretion in 11 healthy controls and in nine patients (19-54 years old; five females and 4 males) rendered athyreotic by surgery and/or 131I for thyroid cancer. Replacement T4 was stopped 47-65 days and subsequent replacement T3 was stopped 33-40 days before the study. All patients were symptomatic with complaints including weight gain, lethargy, and constipation. Deep tendon reflexes had delayed relaxation phase. Serum cholesterol and creatine phosphokinase levels were elevated. Thyroid hormone levels were markedly decreased (means +/- SE; T4: 0.7 +/- 0.3 micrograms/dl; free T4: 0.2 +/- 0.1 ng/dl; T3: 28 +/- 6 ng/dl) and TSH was markedly increased (88 +/- 16 microU/ml). Gastric fractional emptying rate (%/min) and hydrogen ion (H+) output (meq/hr) were determined before and following two sequential stimulations: a 250-ml water load and an intravenous infusion of pentagastrin (6 micrograms/kg/hr). There were no significant differences between controls and athyreotic patients. Our data demonstrated that short-term, profound, thyroid hormone deficiency does not modify gastric emptying or acid output.
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PMID:Gastric secretion and emptying in hypothyroidism. 671 56


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