摘要:

The pathogenesis of autoimmune vasculitis is poorly understood. Understanding the immunologic mechanisms governing this disease requires precise identification of the cells which comprise the lesion. In this report, we have evaluated tissue sections from MRL/lpr mice from 16 to 45 weeks of age, representing all stages of clinical vasculitis. We demonstrate that basophil myelocytes participate in the evolution of the delayed-type hypersensitivity (DTH) response which initiates and perpetuates autoimmune vasculitis in these mice. These findings raise questions regarding the immunologic mechanisms by which basophils develop in this lesion and the interaction of basophils, VSMCs and lymphocytes in vasculitic angiodestruction.

ISSN:0891-6934    

DOI:10.3109/08916939209148455

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

To investigate the specificity of anti HI antibodies peptides from the N- and C-domain of HI and the synthetic oligonucleotide (AT)6were complexed. Circular dichroism (CD) spectroscopy indicated that the free peptides H1(1-16), H1(204-218) and C(121-210) in low salt buffer assume a random structure but become helical when bound to the oligonucleotide. The structured and unstructured HI fragments were then analyzed by enzyme linked immunosorbent assay (ELISA) with anti-Hl antibodies in sera from patients with systemic lupus erythematosis (SLE) and with the monoclonal anti-Hl antibody MRA-12 derived from MLR lpr/lpr autoimmune mice. Binding of these antibodies to HI(204-218) and C was inhibited to a level of 50% when these HI peptides were complexed with (AT)6. When the same antibody was tested with HI fragment GC(34-210), attachment to oligonucleotide (AT)6did not influence antibody binding. Competition studies with liquid phase GC and C antigen against solid phase GC and C indicated that liquid phase GC was more efficient in displacing antibody binding reactivity than liquid phase C. The displacement effect of both liquid phase antigens was greatest against solid phase C. We conclude that anti-Hl autoantibodies are directed against an epitope located near the junction of the G- and C-domain which is exposed and not masked when HI is bound to DNA.

ISSN:0891-6934    

DOI:10.3109/08916939209148456

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

S-Antigen, a photoreceptor cell protein, is highly efficient in inducing experimental autoimmune uveoretinitis (EAU), a severe inflammation of the uveal tract and retina of the eye. S-Antigen and six synthetic peptides, all of which correspond to known T-cell or B-cell recognition sites, were tested for their abiity to induce oral tolerance to EAU in LEW rats. Feeding three 1-mg doses of native S-Antigen or three doses of one synthetic peptide, designated BSA(343-362) (200μper dose), reduced the incidence and severity of EAU induced by immunization with 50μof S-Antigen. Another peptide, BSA(270-289), was able to inhibit EAU only when a low dose (10μ) of the uveitogenic S-Antigen was used to induce EAU. Animals which received 200μdoses of four other immunologically active peptides, BSA(31-51), BSA (143-162), BSA(303-327) and BSA(333-352), were not significantly protected. Furthermore, animals fed BSA(343-362) were significantly less susceptible to EAU induced by adoptive transfer (tEAU) of the uveitogenic R9 T-cell lines. Con A-acti-vated lymphocytes purified from spleens of rats fed peptide BSA(343-362) transferred partial resistance to tEAU induced by adoptive transfer of R9 line cells. The resistance of orally tolerized rats to induction of EAU by adoptive transfer of an activated, pathogenic T-cell line, and the ability of lymphocytes from orally-tolerized animals to transfer resistance to tEAU shows that effector mechanisms can be inhibited by oral feeding as well as the afferent mechanisms reported here and elsewhere. Circulating levels of IgG specific for S-Antigen were not affected by feeding any of the peptides.

ISSN:0891-6934    

DOI:10.3109/08916939209148457

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

The presence and distribution of 7 cytokines was examined immunohistologically in labial salivary gland (LSG) specimens from patients with primary Sögren's syndrome (SS) and control subjects. The cytokines interleukin (IL)-1βIL-6, tumor necrosis factor (TNF)αand interferon (IFN)γwere identified in defined parts of LSG from patients but not in the corresponding parts of control glands: (a) LSG acinar epithelium expressed IL-1β, (b) blood vessels located in both normal LSG stroma and within lymphocytic infiltrates expressed IL-lβ, IL-6 and IFNm`, and (c) lymphocytic infiltrates expressed IL-lβ, IL-6 and TNFα. All four cytokines were expressed by salivary ducts within both patient and control specimens, but with generally greater intensity in patients. IL-lα, IL-4 and TNFβ(lymphotoxin) could not be detected in any of the specimens from patients or controls. The locations of cytokines in LSG suggests possible mechanisms of immunologically mediated parenchymal damage in primary SS.

ISSN:0891-6934    

DOI:10.3109/08916939209148458

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

We have previously reported that a single injection of complete Freund's adjuvant (CFA) can prevent diabetes appearance in diabetes-prone (DP) BB rats. In this study, we investigated further the mechanism of CFA-induced protection from diabetes. We found that adoptive transfer of splenic cells from CFA-treated DP rats into young DP rats protected the latter from diabetes development. This suggested that CFA-induced protection from diabetes resulted from activation of regulatory (suppressor) cells. Cell mixing experimentsin vitroindicated that CFA activated splenic cells with antigen-nonspecific suppressor activity (suppression of lymphoproliferative responses to lipopolysaccharide and to allogeneic splenic cells). Fractionation of splenic cells on Percoll revealed that the suppressor activity resided in low density cells relatively depleted of T-cells, B-cells, macrophages and NK cells. These results suggest that non-specific (natural) suppressor cells in CFA-treated BB rats may be responsible for suppressing autoimmune responses and preventing insulitis and diabetes development.

ISSN:0891-6934    

DOI:10.3109/08916939209148459

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Despite extensive study, the pathogenic mechanisms of Behçet's disease remain uncertain. The ocular inflammation caused by this disease is severe, often causing significant visual loss and, although the nature of the cellular infiltrate has been examined in many of the involved organs, the infiltrating cells in inflamed eyes have not.To investigate the mechanisms involved in perpetuating the ocular inflammation, five enucleated eyes from patients with Behçet's disease were examined by immunohistochemical staining using a panel of monoclonal and polyclonal antibodies. Control eyes from patients with chronic intraocular inflammation from other causes were also examined.Cellular infiltrates were a consistent finding in choroid and periretinal scar tissue, formed almost entirely by mononuclear cells. T lymphocytes were found to predominate (largely the CD4+subset). B lymphocytes and NK cells were infrequent findings but macrophages were present in significant numbers. No complement or immunoglobulin deposits were found. Infiltrating lymphocytes and macrophages were HLA DR positive. Retinal vacular and retinal pigment epithelium were only occasionally positive.Our findings suggest that cell mediated immunity, rather than immune complex deposition is responsible for the perpetuation of the ocular inflammation in Behçet's disease and that CD4+T lymphocytes play a central role in this.

ISSN:0891-6934    

DOI:10.3109/08916939209148460

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Levels of CD5+B lymphocytes were assayed in a large family study of Primary Sögren's syndrome. There was no significant difference in CD5 expression by index cases or their relatives when compared to controls. No association between CDS expression, serological abnormalities or HLA haplotype was found and, furthermore, no evidence of linkage with HLA was observed. There was, however, variation in the expression of CD5+B cells between the families. Levels in spouses were lower and reached statistical significance. The role for genetic and environmental factors influencing CD5 expression is discussed. Any genetic influence does not appear to involve the HLA region or genes in linkage disequilibrium.

ISSN:0891-6934    

DOI:10.3109/08916939209148461

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Thyroid-associated ophthalmopathy (TAO) is one of the most vexing problems in endocrinology but its relationship to thyroid autoimmunity is becoming more clear with the realisation that almost all patients with Graves' disease have this condition and almost all patients with ophthalmopathy have some form of thyroid involvement. This suggests cross reactivity between thyroid and retrobulbar antigens, of which one potential candidate has recently been cloned. Together with new information on predisposing factors and the important role of the retrobulbar fibroblasts, these developments shed new light on the aetiology and pathogenesis of this enigmatic disorder.

ISSN:0891-6934    

DOI:10.3109/08916939209148462

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916939209148463

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916939209148464

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor