摘要:

Adoptive transfer of experimental allergic encephalomyelitis (EAE) is enhanced afterin vitroculture of myelin basic protein (BP)-sensitized lymphoid cells with BP. Addition of lipopolysaccharide (LPS) to the culture further augments transfer of EAE to a level 5 times greater than that achieved with cells activated only with BP. Neither the proliferative response of a BP-specific cell line nor the production of IL-2 by BP-sensitized lymphoid cells in response to BP was augmented by the addition of LPS to the culture. Augmentation of EAE was also observed if recipients received simultaneous injections of BP-sensitized lymph node cells (BP/LNC) cultured with BP (BP-activated) and normal spleen cells cultured independently with LPS (LPS/Spl-C). To analyze the effect of contact between these two cell populationsin vivo, we mixed the two cell populationsin vitroat reduced cell concentrations. When BP-activated BP-LNC were mixed with LPS-Spl-Cin vitro, a marked synergistic proliferative response was observed. Irradiation of BP-activated BP/LNC abrogated this synergistic response, whereas irradiation of LPS/Spl-C did not, suggesting that the proliferating population was in the BP/LNC and that the LPS/Spl-C enhanced their proliferation. These results indicate that LPS exerts its effect through BP-nonspecific cells and that these cells enhance transfer of EAE by augmenting the proliferation of the BP-specific cellsin vivoafter transfer.

ISSN:0891-6934    

DOI:10.3109/08916938908997153

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

BALB/cByJ substrain mice are highly susceptible to the induction of EAO whereas BALB/cJ mice are resistant. BALB/cJ mice have been reported to have elevated levels of serum T, which may account for disease resistance in light of its purported immunosuppressive effects. Serum T levels were determined by radioimmunoassay on 40 BALB/cByJ and 41 BALB/cJ age matched male mice. Our results indicate that the two substrains do not differ significantly from each other in their mean serum T levels (BALB/cByJ-4.50ng/ml and BALB/cJ-3.16ng/ml; p = 0.601) suggesting that the EAO resistant phenotype exhibited by BALB/cJ mice is not a result of the immunosupressive effects of T.

ISSN:0891-6934    

DOI:10.3109/08916938908997154

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

The purpose of the present study was to determine whether patients with euthyroid Graves’exophthal-mopathy have an impaired NK cell function compared to patients with Graves’hyperthyroidism and healthy controls.The NK cell activity measured against K562 target cells was significantly suppressed (p<0.01) in patients with euthyroid Graves’ophthalmopathy, whereas the NK cell activity of patients with Graves’hyperthyroidism was not. Although interferon-α, interleukin-2 and indomethacin significantly enhanced (p<0.01) the NK cell activity in all three groups, none of these agents fully restored the defective NK cell activity in euthyroid Graves’ophthalmopathy. The concentrations in the blood of large granular lymphocytes and CD 16 positive cells did not differ between the three groups, furthermore an immunosuppressive serum factor was not detected. The number of effector/target cell conjugates did not differ between patients and controls, whereas the interferon-α-induced production of a soluble natural killer cytotoxic factor (NKCF) with specificity for NK sensitive target cells was suppressed in patients with Graves’euthyroid ophthalmopathy. We conclude that one of the mechanisms underlying the defective NK cell activity in patients with euthyroid ophthalmopathy may be an impairment of the release of NKCF from the NK cells.

ISSN:0891-6934    

DOI:10.3109/08916938908997155

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

IgG antibodies to insulin are present in insulin-treated patients and are detected in the prodrome of untreated type I diabetes. Sporadic reports of autoantibodies to insulin suggest that they are also present in other disorders. To establish the incidence of insulin autoantibodies in other endocrine and autoimmune diseases an ELISA was used to examine sera from 529 subjects with no prior insulin therapy. These untreated patients included: normal controls (adults and children), newly-diagnosed type I diabetes, first-degree relatives of diabetics, type II diabetes, Graves' hyperthyroidism, and systemic lupus erythematosus. As a positive control group, 280 insulin-treated patients were studied. Measurement of IgG antibodies by direct binding to insulin coated plates was complicated by differences between adult and pediatric populations and by overlap of binding between treated and untreated subjects. Competitive inhibition with excess soluble human insulin overcame these problems and permitted identification of insulin specific binding. Using this approach insulin antibodies were most frequent in insulin-treated diabetics (98%) and in type I diabetics (37%) prior to treatment. The absolute numbers of subjects with insulin autoantibody in the other groups differed depending upon whether a cut-off for binding (mean + 2SD of controls) or for insulin inhibition of binding (45%) was used. Regardless of the criteria used there were subjects (2-24%) in all groups tested with circulating insulin-specific IgG autoantibody detected by ELISA. These low level antibodies detected in solid phase assays may be part of the normal immune repertoire.

ISSN:0891-6934    

DOI:10.3109/08916938908997156

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Aberrant MHC Class II antigen expression and the nature of the infiltrating lymphoid cells were studied by immunohistochemical techniques in liver biopsies from 37 patients with Primary biliary cirrhosis (PBC) (11 histological stage I, 13 stage II-III, 13 stage IV) and 15 patients with chronic non autoimmune liver disease. Bile duct epithelial cells expressed HLA-DR, DP and DQ antigens in biopsies from patients with early (Stage I) PBC and less frequently in the late cirrhotic phases of the disease (Stage IV); these observations support the hypothesis that induction of Class II antigens on epithelial cells may be involved in initiating autoimmune responses towards bile duct components. The presence of cytotoxic/suppressor T cells around the bile ducts in Stage I suggests a role for cell mediated destruction of the ducts at this early stage. The nature of the chronic inflammatory cell infiltrate in the portal tracts, periportal areas and lobular parenchyma does not establish the mechanism(s) involved in disease progression. However, the lack of Class II antigen expression on hepatocytes is compatible with the hypothesis that hepatocellular damage is non-specific and may be secondary to the initial bile duct injury.

ISSN:0891-6934    

DOI:10.3109/08916938908997157

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

In inflammatory disease of the central nervous system (CNS), oligoclonal bands of immunoglobulin with restricted heterogeneity can often be observed in cerebrospinal fluid (CSF) samples. These antibodies can be directed against the disease inducing pathogen or might be autoreactive and involved in the process of brain inflammation and demyelination. We used a molecular biology approach to characterize these antibody responses in patients with Lyme disease. This disorder is caused by infections with the spirocheteBorrelia burgdorferiwhich is transmitted by ticks. Lyme disease can be associated with neurological symptoms due to inflammation of the central and peripheral nervous system. Phageλgt!! expression libraries fromB. burgdorferiand human brain were screened with cerebrospinal fluid antibody probes from patients with Lyme disease. We obtained recombinant phage clones encoding antigenic proteins from bothB. burgdorferiand human CNS libraries. Thus, in this study two patients with chronic Lyme disease produced antibodies against recombinantB. burgdorferias well as against CNS proteins, and the generation of this transient autoimmune response might be essential to the development of demyelinating disease.

ISSN:0891-6934    

DOI:10.3109/08916938908997158

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916938908997159

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916938908997160

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor