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At least 361 records · Page 20Linked to original sources
PubMed1999

[Latent autoimmune (type I) diabetes mellitus in adults. Part. II. Association of HLA antigens, status of cellular immunity and occurrence of other autoimmune diseases].

AIM OF STUDY: To assess some immunological and immunogenetic aspects in patients with latent autoimmune (Type-1) diabetes mellitus (DM) of adults (LADA). SUBJECTS: 24 patients with LADA, 11 patients with Type-2 DM and 20 healthy volunteers (Pilot study). PARAMETERS TESTED: HLA-DRB1* and HLA-DQB1* alleles, parameters of cellular immunity (CD4+, CD8+, CD3/HLA-DR+, CD8/HLA-DR+, CD45RA+[CD4], CD16+CD56), CD19+, IL-4, INF-gamma and organ specific (OSA) autoantibodies (against thyroid gland, gastric parietal cells, tubuli, basal membranes of glomerulus, AMA and ABBA). RESULTS AND DISCUSSION: Type-1 DM HLA-DRB1* and HLA-DQB1* risk alleles have been found in a majority of patients with LADA. The most frequent were HLA-DRB1*0301 and DQB1*0201. Assessement of parameters of cellular immunity and cytokine profiles (IL-4 a INF-gamma) in peripheral blood did not reveal any contribution to a differentiation between Type-1 and Type-2 DM). We confirmed increased occurence of OSA in patients with LADA, what stress importance of routine screening for OSA in patients with LADA.

Aged↗
PubMed2004

Autoimmune and non-autoimmune hyperthyroidism in pediatric patients: a review and personal commentary on management.

Here we review the etiology, diagnosis, differential diagnosis, and clinical presentation of hyperthyroidism in neonates/infants, children, and adolescents and the standard and adjunct modalities used for its treatment. The most common cause of hyperthyroidism in pediatric patients is Graves' disease. The main options for its management include antithyroid drugs, surgery, and radioiodine therapy. Despite collective experience covering more than 4 decades in the management of hyperthyroidism in children, controversy still abounds regarding the choice of treatments. None of the current treatment options is ideal. Each has risks and selection should be tailored to individual patients, especially in view of the absence of large, prospective, randomized outcome studies. Finally, we discuss the diagnosis and management of less common causes of pediatric hyperthyroidism, including non-autoimmune causes in neonates, autonomously functioning thyroid adenomas, destructive thyroiditis, excessive or inappropriate thyroid-stimulating hormone production, excessive ingestion of thyroid hormone and exposure to large, stable iodine loads.

Adolescent↗
PubMed1983

Autoimmune effector cells. V.A monoclonal antibody specific for rat helper T lymphocytes inhibits adoptive transfer of autoimmune encephalomyelitis.

The in vitro activation of spleen cells from donor rats immunized with myelin basic protein results in enhanced adoptive transfer of experimental allergic encephalomyelitis to syngeneic recipients. In this study, adoptive transfer was inhibited when monoclonal antibody W3/25, which defines an antigen on rat helper T lymphocytes, was included in the in vitro cultures. Partial inhibition was achieved with monoclonal antibody OX-3, which recognizes la antigen, whereas other anti-T cell monoclonal reagents were ineffective. These results support the conclusion that W3/25+T cells play an essential role in the induction of this autoimmune response.

Animals↗
PubMed1982

Analysis of recombinant inbred lines derived from "autoimmune" (NZB) and "high leukemia" (C58) strains: independent multigenic systems control B cell hyperactivity, retrovirus expression, and autoimmunity.

The relationship of B cell hyperactivity and retrovirus expression to other autoimmune traits were examined in recombinant inbred (N X 8 RI) lines derived from NZB and C58 progenitor strains. Although both NZB and C58 mice expressed high levels of xenotropic virus, the RI lines segregated in virologic phenotype, as high or low expressors of the endogenous virus. The expression of the C58-derived ecotropic virus occurred in only one-half of the RI lines, and its expression in the remaining lines of mice appeared to be suppressed by the NZB-derived allele at the Fv-1 locus. The inheritance of B lymphocyte abnormalities of the NZB progenitor strain was investigated by studying spontaneous and SRBC-induced production of IgM by the spleen cells of the RI lines. These two phenotypes of B cell hyperactivity were found to be determined by independently segregating genes and they were not linked to immunoglobulin structural gene loci. The strain distribution patterns of virus expression and B cell hyperactivity in the RI lines did not match with each other or with the inheritance patterns of other immunologic abnormalities, such as defective AMLR and production of autoantibodies.

Animals↗
PubMed1981

Vaccination against autoimmune encephalomyelitis (EAE): attenuated autoimmune T lymphocytes confer resistance to induction of active EAE but not to EAE mediated by the intact T lymphocyte line.

Autoimmune encephalomyelitis (EAE) can be induced in genetically susceptible rats by active immunization against myelin basic protein (BP) or by passive transfer or anti-BP lymphocytes. We have developed in vitro lines of T lymphocytes reactive only against BP that produce EAE upon i.v. inoculation of syngeneic rats. The object of the present study was to learn whether attenuated anti-BP line cells could be used to vaccinate rats against passive as well as active EAE. We inoculated rats i.v. with anti-BP line cells that were attenuated by irradiation or treatment by mitomycin C. A single inoculation was sufficient to protect about 70% of rats from subsequent EAE induced actively. However, even repeated vaccination could not protect against EAE mediated by passive transfer of anti-BP line cells. Thus, attenuated cells of EAE effector lines cannot vaccinate the autoreactive effects of preformed effector T lymphocytes.

Animals↗
PubMed2001

Characterization of BALB/c mice B lymphocyte autoimmune responses to skin basement membrane component type XVII collagen, the target antigen of autoimmune skin disease bullous pemphigoid.

Bullous pemphigoid is an autoimmune blistering skin disease characterized by IgG autoantibodies targeting the skin basement membrane component type XVII collagen (BPAg2). To gain understanding of the disease's induction phase, we subcutaneously immunized adult BALB/c mice with peptides of human and/or the murine-equivalent BPAg2 pathogenic NC16A domain. Female mice were injected with peptides (human, murine, or combined human and murine), or PBS control emulsified in CFA, on a four-week interval. At the fourth and subsequent immunizations, all peptide-immunized mice were given murine peptides. Two weeks after the sixth immunization, ELISA detected IgG circulating autoantibodies against self peptides in 92% (47/51) of mice immunized with murine peptides; whereas none of the preimmune sera or the sera from PBS control-immunized mice reacted to the self peptides. In four mice their autoantibodies labeled mouse skin basement membrane. Breaking B-cell tolerance to BPAg2 sets the first step in dissecting the disease's induction phase.

Amino Acid Sequence↗
PubMed2006

Evidence from autoimmune thyroiditis of skewed X-chromosome inactivation in female predisposition to autoimmunity.

The etiologic factors in the development of autoimmune thyroid diseases (AITDs) are not fully understood. We investigated the role of skewed X-chromosome inactivation (XCI) mosaicism in female predisposition to AITDs. One hundred and ten female AITDs patients (81 Hashimoto's thyroiditis (HT), 29 Graves' disease (GD)), and 160 female controls were analyzed for the androgen receptor locus by the HpaII/polymerase chain reaction assay to assess XCI patterns in DNA extracted from peripheral blood cells. In addition, thyroid biopsy, buccal mucosa, and hair follicle specimens were obtained from five patients whose blood revealed an extremely skewed pattern of XCI, and the analysis was repeated. Skewed XCI was observed in DNA from peripheral blood cells in 28 of 83 informative patients (34%) as compared with 10 of 124 informative controls (8%, P<0.0001). Extreme skewing was present in 16 patients (19%), but only in three controls (2.4%, P<0.0001). The buccal mucosa, and although less marked, the thyroid specimens also showed skewing. Analysis of two familial cases showed that only the affected individuals demonstrate skewed XCI patterns. Based on these results, skewed XCI mosaicism may play a significant role in the pathogenesis of AITDs.

Adult↗
PubMed1991

Clonotypic analysis of anti-acetylcholine receptor antibodies from experimental autoimmune myasthenia gravis-sensitive Lewis rats and experimental autoimmune myasthenia gravis-resistant Wistar Furth rats.

A single immunization of Lewis rats with purified acetylcholine receptor (AChR) emulsified in adjuvant typically stimulates the production of oligoclonal AChR-reactive antibodies (as demonstrated by IEF) dominated by the IgG2a subclass, of moderate but clonotypically heterogeneous relative Ag-binding avidity, and capable of inducing symptoms of experimental autoimmune myasthenia gravis. Although similar immunization of Wistar Furth rats produces AChR-reactive antibodies with similar characteristics of clonotypic heterogeneity, avidity, and isotype expression, no detectable signs of AChR-dependent muscle impairment is observed. This contrasts the ability to induce impaired AChR function upon the passive transfer of pre-formed Lewis anti-AChR antibodies into naive Wistar Furth rats, suggesting that disease resistance in this model is not conferred at the level of the AChR itself. Moreover, if more aggressive immunization protocols are used (i.e., multiple injections of AChR), a transient breakthrough of AChR-dependent muscle dysfunction can be induced directly in the Wistar Furth strain indicating that the potential for the production of disease-causing antibodies does exist in the Wistar Furth repertoire. IEF analysis of Wistar Furth anti-AChR antibodies has revealed that hyperimmunization results in modified antibody clonotype expression that might explain changing expression of disease symptoms; however, explanations for the apparent "resistance" of Wistar Furth rats to disease induction are likely to be complex.

Animals↗
PubMed1989

Vaccination against experimental autoimmune encephalomyelitis using a subencephalitogenic dose of autoimmune effector cells (1). Characteristics of vaccination.

We previously reported that rats could be vaccinated against EAE by inoculation with 10(7) anti-basic protein (anti-BP)-activated T cells raised as long-term lines. The activated T lines were irradiated (1,500 rads) to prevent them from causing EAE. We now report that a single inoculation of 10(4) or fewer cells of an activated anti-BP T-cell line did not cause clinical EAE but rather induced marked resistance to EAE produced by adoptive transfer of the anti-BP T cells. Resistance was less effective against EAE induced by active immunization to BP. Vaccination was immunologically specific, long lasting, and could be effected by various routes of administration.

Animals↗