摘要:

Heat shock protein 60 expression in the thyrocytes of Hashimoto's thyroiditis and Graves' disease was studied immunohistochemically. Thyrocytes of Hashimoto's thyroiditis showed high expression of heat shock protein 60 not only in tall eosinophilic-cells but also in low and flattened cells, although the former was stained with moderate to strong staining intensity and the latter weakly to moderately. Follicular cells around lymphoid cell follicles were stained more intensely, whereas cells apart from lymphoid cell follicles were stained weakly to moderately. In Graves' disease, only follicular cells around lymphoid cell follicles were stained with varying intensities. Since the pattern in all positive staining was granular, it was thought that heat shock protein 60 over-expressed in thyrocytes located on mitochondria.To investigate the immunological role of overexpression of self heat shock protein 60 in the thyrocytes of Hashimoto's thyroiditis,γσTCR+T-cells in the tissue and the IgG class of anti-self heat shock protein 60 antibodies were studied.γσTCR+T-cells were detected among lymphoid cells scattered in interfollicular connective tissue. No difference in antibody level was seen among subjects with Hashimoto's thyroiditis, Graves' disease and normal subjects. Self heat shock protein 60 overexpression in the thyrocytes of Hashimoto's thyroiditis may play a disease-modifying role, although it does not influence the anti-self heat shock protein 60 antibody level.

ISSN:0891-6934    

DOI:10.3109/08916939608994721

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

The present study was made to investigate the effect of mizoribine (MZR), an imidazole nucleoside immunosuppressant, on pulmonary lesions and immunological mode of action of MRL/1pr/1pr mice. Four-week-old female MRL/1pr/1pr mice were injected subcutaneously with 20 mg/kg body weight of MZR every other day. For control, mice were given phosphate-buffered saline (PBS) every other day. MZR caused the delay in the histological development of peribronchial and perivascular lymphocytic infiltrations in the lungs of MRL/1pr/1pr (MRL/1pr) mice. And then, MZR suppressed the number of immunoglobulin (Ig) (IgG and IgM) secreting B cells and anti-DNA-secreting B cells in the spleen of MRL/1pr/1pr mice. The above data indicate that MZR could be useful for the treatment of pulmonary lesions associated with autoimmune disorders such as systemic lupus erythematosus (SLE).

ISSN:0891-6934    

DOI:10.3109/08916939608994722

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

Immunization of albino LEW rats with a retinal soluble antigen (S-antigen) induces experimental autoimmune uveoretinitis (EAU) which shows clinical features resembling those of human uveitis. Several uveitogenic epitopes have been identified in the antigen. This study reports that an intratesticular injection of low doses of a uveitogenic eicosapeptide (P343-362) of S-antigen prior to immunization with the same peptide prevented the onset of EAU by inducing systemic tolerance, designated orchidic tolerance. Splenic lymphocytes of both CD4+and CD8+subsets from tolerized rats transferred orchidic tolerance to syngeneic recipients and protected them from subsequent EAU induction. Orchidic tolerance elicited by low antigen dosage was mediated, in part, by active suppression due to suppressor or regulatory cells. At high antigen doses, however, regulatory activity was reduced possibly due to the induction of anergy in regulatory cells, and EAU severity increased. The CD4+regulatory T cells from tolerized rats showed enhanced expression of IL-4 mRNA compared with CD4+cells from control rats. Increased immunoreactivity for IL-4, IL-10 and TGF-βwas observed in the spleen and lymph nodes of tolerized animals. The results suggest that orchidic tolerance induced by low doses of P343–362 is mediated in part by CD4+regulatory cells secreting Th2 cytokines.

ISSN:0891-6934    

DOI:10.3109/08916939608994723

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

The tryptophan dimer 1,1′-ethylidenebis[L-tryptophan] was identified as a contaminant of tryptophan preparations associated with Eosinophilia-Myalgia Syndrome. In this paper, we describe experiments examining the hypothesis that 1,1′-ethyli-denebis[L-tryptophan] acts as an amino acid analog replacing L-tryptophan during the synthesis of proteins. We propose further that proteins containing 1,1′-ethylidenebis[L-tryptophan] are rejected in an autoimmune process identified clinically as Eosinophilia-Myalgia Syndrome.Rabbit reticulocyte lysates containing an estimated 1μM L-tryptophan were used to assay the ability of 1,1′-ethylidenebis[L-tryptophan] to compete with3H-L-tryptophan for incorporation into proteins translated from BMV RNA. 1,1′-Ethylidenebis[L-tryptophan] in concentrations of 40, 80 and 110μM reduced lysate3H-L-tryptophan incorporation to 81%, 76% and 75% of control incorporation obtained in the absence of 1,1′-ethylidenebis[L-tryptophan]. In the presence of 20μM L-tryptophan, 110μM 1,1′-ethylidenebis(L-tryptophan] reduced3H-L-tryptophan incorporation to 56% of control incorporation. In contrast, ethyl-L-tryptophan did not significantly reduce3H-L-tryptophan incorporation. In the presence of 110μM 1,1′-ethylidenebis[L-tryptophan] and 20μM L-tryptophan,3H-L-leucine incorporation was not significantly reduced compared to incorporation in the absence of 1,1′-ethylidenebis[L-tryptophan], demonstrating that proteins were translated to full length during elongation. These findings suggest that 1,1′-ethylidenebis[L-tryptophan], but not ethyl-L-tryptophan, reduced3H-L-tryptophan incorporation into proteins by substituting for L-tryptophan rather than by causing premature termination or significant slowing of nascent protein chains.In further experiments, the ethylidene bridge of 1,1′-ethylidenebis[L-tryptophan] was labeled during synthesis with14C-acetaldehyde.14C-1,1′-ethylidenebis[L-tryptophan] was added to rabbit reticulocyte lysates containing BMV RNA to a concentration of 110μM 1,1′-ethylidenebis[L-tryptophan]. On SDS-PAGE gels, bands of14C-labeled proteins were detected at the 5 band positions expected from BMV RNA; i.e., at approximately 100, 97, 35, 20 and 15 kD. We conclude from these experiments that trytophanyl t-RNA synthetase can activate and attach 1,1′-ethylidenebis[L-tryptophan] to tryptophanyl-t-RNA and that 1,1′-ethylidenebisll-tryptophan] can be incorporated into proteins in place of L-tryptophan.To determine whether Eosinophilia-Myalgia Syndrome was associated with sensitization to 1,1′-ethylidenebis[L-tryptophan], we constructed artificial haptens to mimic proteins containing 1,1′-ethylidenebis[L-tryptophan] residues. Haptens were synthesized by coupling 1,1′-ethylidenebis[L-tryptophan], ethyl-L-tryptophan or L-tryptophan to albumin with glutaraldehyde. Peripheral blood lymphocytes were isolated from patients stably recovered from Eosinophilia-Myalgia Syndrome for 2 yr or more and used in proliferation assays against lymphocytes from controls to determine if they were immunosensitive to synthesized haptens. Only one out of the five recovered Eosinophilia-Myalgia Syndrome patients demonstrated significant reactivity to the synthesized hapten containing 1,1′-ethylidenebis[L-tryptophan]. This patient also demonstrated an increased reactivity to the synthesized hapten containing L-tryptophan. A second recovered Eosinophilia-Myalgia Syndrome patient demonstrated increased sensitivity to the synthesized hapten containing ethyl-L-tryptophan. These results provide inconclusive evidence that incorporated 1,1′-ethylidenebis[L-tryptophan] provides an immunogenic stimulus. However, the synthesized haptens may not have sufficiently mimicked the configurations of proteins containing 1,1′-ethylidenebis[L-tryptophan] residues to test for sensitization or sensitization could have been lost in recovered patients following corticosteroid treatment and the turnover of affected proteins.

ISSN:0891-6934    

DOI:10.3109/08916939608994724

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

Previous studies have suggested that there may be a link between Turner's syndrome and autoimmunity. The numbers involved in these studies have tended to be small and few studies have included family members. This study has compared the incidence of thyroid antibodies in the serum of 60 patients with Turner' syndrome and 50 of their mothers with 127 controls. Total T4 and TSH levels were also measured.Of the 60 patients with Turner's syndrome 18 (30%) were positive for either thyroid peroxidase (TPO) and/or thyroglobulin antibodies. The peak incidence of thyroid antibodies occurred at 13 years of age. 11 (22%) of the mothers were also antibody positive. The incidence of thyroid antibodies was significantly higher in both the patients with Turner's Syndrome (30 vs 1.7% p<0.001) and their mothers (22 vs 6.6% p<0.05) than in the control groups.The increased incidence of thyroid antibodies found in these patients and their mothers confirms that there is an association between Turner's Syndrome and autoimmunity. However unlike previous studies we found more patients were positive for thyroglobulin than TPO antibodies.

ISSN:0891-6934    

DOI:10.3109/08916939608994725

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

The present study investigated the expressed number of CR1 on erythrocytes (E) in relationship of the CR1 density genotype from 46 patients with systemic lupus erythematosus (SLE) and 47 healthy volunteers. The CR1 genotype was determined by a method based on polymerase chain reaction (PCR) amplification of the genomic DNA fragment of 1.8 kb separated byHindIIIendonuclease digestion and agarose gel electrophoresis. Our data supported the earlier results that the number of binding sites/E for monoclonal anti-CR1 decreased among SLE patients compared with normal individuals having the same alleles for the CRUE density. At the same time the novelty of our recent results was that the decreased expression of CR1 on E correlated significantly with kidney involvement in patients homozygous for the CR1/E high density allele (HH). These data suggest that the deficiency of the detectable number of CR1 on erythrocytes is acquired in this SLE population.

ISSN:0891-6934    

DOI:10.3109/08916939608994726

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916939608994727

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor