Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reports the use of direct immunofluorescent technique in diagnoses of 80 cases in which 5 kinds of diseases of the oral mucous membrane are included. The results demonstrate that fibrinogen is deposited in basement membrane zone in 100% of lichen planus cases and 21.4% and 75.0% in chronic lupus erythematosus and benign lymphoid hyperplasia respectively. In leukoplakia and chronic infection it is negative. Therefore, the direct immunofluorescent technique is likely a reliable method for diagnosis of certain kinds of diseases of the oral mucous membrane.
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PMID:[Direct immunofluorescent technic of analyzing fibrinogen in the differential diagnosis of certain diseases of the oral mucous membrane]. 250 18

Monoclonal antibody to L3T4 has been used successfully to suppress autoimmunity in the New Zealand black/New Zealand white F1 (B/W) mouse model for systemic lupus erythematosus. To clarify the immunopathology of murine lupus and determine the effects of anti-L3T4 treatment on the cellular composition and histopathology of lymphoid organs, we examined the distribution of lymphocyte subsets in cryostat sections of the thymus, spleen, and lymph nodes of B/W mice. Immunohistologic specimens were obtained from female B/W mice that had received weekly intraperitoneal injections of either rat monoclonal antibody to L3T4 (2 mg/mouse/week) or phosphate buffered saline (200 microliters/mouse/week) from age 5 months until euthanasia at 8 months. B and T cell domains in each organ were identified on serial sections with monoclonal antibody directed against B220 (all B cells), Thy-1.2 (all T cells), L3T4 (helper T cells), and Ly-2 (cytotoxic/suppressor T cells). In control mice, striking cytoarchitectural abnormalities were identified in the thymuses, and the spleen and lymph nodes were hypertrophied relative to anti-L3T4 treated mice. Thymic abnormalities included amplification of medulla, formation of thymomas, and cortical atrophy. Amplified medullary regions and thymomas in B/W mice contained numerous B cells and L3T4+ T cells but few Ly-2+ T cells. The enlarged spleens and lymph nodes of control mice consisted of numerous secondary follicles with germinal centers containing an unusual subpopulation of T cells that expressed L3T4 but not Thy-1.2. In contrast, mice treated with anti-L3T4 did not develop histopathologic changes characteristic of systemic lupus erythematosus in any organ. However, treatment depleted L3T4+ cells from the spleen and lymph nodes, and it modulated the expression of L3T4 by thymocytes. These observations demonstrate that treatment with anti-L3T4 not only interferes with L3T4-dependent T cell functions, but it also prevents progressive abnormalities in lymphoid tissue in lupus-prone B/W mice. This preservation of normal lymphoid structure may contribute to the beneficial effects of anti-L3T4 on autoimmunity.
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PMID:Treatment of murine lupus with monoclonal antibody to L3T4. II. Effects on immunohistopathology of thymus, spleen, and lymph node. 252 96

An almost universal side effect of long-term therapy with procainamide is the appearance of serum autoantibodies and less frequently a syndrome resembling lupus erythematosus. Previous studies demonstrated that procainamide-hydroxylamine (PAHA), a metabolite generated by hepatic mixed function oxidases, was highly toxic to dividing cells, but evidence that PAHA could be formed in the circulation was lacking. This study examines the capacity of neutrophils to metabolize procainamide to reactive forms. Neutrophils activated with opsonized zymosan were cytotoxic only if procainamide was present, whereas N-acetyl procainamide, which does not induce autoimmunity, was inert in this bioassay. PAHA was detected by HPLC in the extracellular medium if ascorbic acid was present. Generation of PAHA and cytotoxic procainamide metabolites was inhibited by NaN3 and catalase but not by superoxide dismutase, indicating that H2O2 and myeloperoxidase were involved. Nonactivated neutrophils and neutrophils from patients with chronic granulomatous disease did not generate cytotoxic PAHA, demonstrating that H2O2 was derived from the respiratory burst accompanying neutrophil activation. These conclusions were supported by results of a cell-free system in which neutrophils were replaced by myeloperoxidase and H2O2 or an H2O2 generating system. These studies demonstrate the capacity of neutrophils to mediate metabolism of procainamide and establish the role of myeloperoxidase released during degranulation and H2O2 derived from the respiratory burst in the direct cooxidation of procainamide to PAHA. The profound biologic activity of this metabolite and its possible generation within lymphoid compartments implicate this process in the induction of autoimmunity by procainamide.
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PMID:Metabolism of procainamide to the cytotoxic hydroxylamine by neutrophils activated in vitro. 253 97

To evaluate the degree of genetic polymorphism of the V kappa repertoire in systemic lupus erythematosus (SLE), we performed Southern blot hybridizations with human gene probes corresponding to the four human V kappa gene families. In a comparative analysis, non-lymphoid cell DNA samples from three patients with idiopathic SLE, eight subjects with susceptibility to drug-induced lupus and seven control individuals were digested with the restriction endonucleases Bam HI, Bg 1 II, Eco RI and Hind III, and hybridized sequentially to the four V kappa family-specific probes. The restriction patterns on Southern blots revealed a low degree of polymorphism of the human V kappa gene repertoires of SLE patients and control individuals. This analysis, together with previous parallel studies of the V kappa locus in lupus-prone mice, implies that autoantibody hyperproduction in lupus is not associated with major modifications in the structure or genomic organization of immunoglobulin light chain genes.
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PMID:Restriction fragment length polymorphism analysis of the V kappa locus in human lupus. 257 7

Mice of the genetically different BXSB and MRL/lpr strains develop murine lupus spontaneously at about three months of age. Polyclonal B-cell activation is thought to play a major role in the development of the syndrome in each strains, but the immunological events which lead to this activation are not known. We therefore examined the immune characteristics of mice aged 10-16 weeks, at the onset of the disease. We found consistent abnormalities in the percentages of lymphocyte sub-populations in both male BXSB, and male and female MRL/lpr mice. In particular, the ratio of helper to suppressor/cytotoxic T cells was found to be significantly lower in male BXSB, and in male and female MRL/lpr mice than in normal, control, DBA2 mice. Significant increases in serum IgG and IgA concentrations, indicative of polyclonal B cell activation, were present in each strain. The histological appearance of the lymphoid organs and the functional responses to mitogen stimulation were, however, distinctly different. We conclude that defective immunoregulation is likely to be significant in the initiation of murine lupus, since it is detectable at the onset of disease in two genetically distinct strains. It may be associated, however, with different immunological phenomena in strains of different genetic backgrounds.
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PMID:A search for common immunological abnormalities at the onset of murine lupus in two genetically different strains. 257 49

In normal human epidermis HLA-DR-antigen is only present on Langerhans' cells and the acrosyringeal epithelium. We investigated the distribution of HLA-DR-antigen in 78 specimens of various skin diseases by an immunoperoxidase method using a monoclonal anti-HLA-DR antibody. HLA-DR-antigen bearing keratinocytes were not only found in lichen planus and mycosis fungoides, as it has been referred previously, but were also observed in some cases of cutaneous B-cell lymphoma, pseudolymphoma, lupus erythematosus, parapsoriasis en plaque, bullous pemphigoid, drug reaction, contact dermatitis, actinic keratosis and verrucous carcinoma. Direct contact of lymphoid cells with keratinocytes was not necessary for Ia-antigen expression.
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PMID:HLA-DR-antigen bearing keratinocytes in various dermatologic disorders. 257 18

A case of lupus lymphadenitis with frozen section immunohistologic studies is presented. Clinically, the patient had well-documented systemic lupus erythematosus (SLE) when rapid development of generalized lymphadenopathy raised the possibility of a diagnosis of malignant lymphoma. Histologically, the findings of paracortical foci of necrosis and hematoxylin bodies were diagnostic of SLE. Granulocytes were absent. Monoclonal antibodies applied to frozen sections demonstrated two predominant cell populations within and surrounding the paracortical zones of necrosis: OKM1+, Leu-M1+ histiocytes and OKT8+, Leu-4+ T cytotoxic/suppressor cells. In the lymph node not involved by necrosis, lymphoid follicles were composed of polytypic B cells and the interfollicular regions of T cells. Leu-3a+, Leu-4+ T helper/inducer cells outnumbered T cytotoxic/suppressor cells in a 3:1 ratio. Since lupus lymphadenitis may closely resemble histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto, particularly if hematoxylin bodies are not found, we compared the findings in this case with findings of cases of histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto reported in the literature. The immunologic findings in both diseases are similar. We conclude that immunologic studies using frozen sections are probably of no help in differentiating between these two disorders when histologic findings are not conclusive.
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PMID:Lupus lymphadenitis: report of a case with immunohistologic studies on frozen sections. 265 95

Treatment with total lymphoid irradiation (TLI) and corticosteroids markedly reduced activity of systemic lupus erythematosis in 10 patients with diffuse proliferative lupus nephritis (DPLN) complicated by a nephrotic syndrome. Physiologic and morphometric techniques were used serially before, and 12 and 36 mo post-TLI to characterize the course of glomerular injury. Judged by a progressive reduction in the density of glomerular cells and immune deposits, glomerular inflammation subsided. A sustained reduction in the fractional clearance of albumin, IgG and uncharged dextrans of radius greater than 50 A, pointed to a parallel improvement in glomerular barrier size-selectivity. Corresponding changes in GFR were modest, however. A trend towards higher GFR at 12 mo was associated with a marked increase in the fraction of glomerular tuft area occupied by patent capillary loops as inflammatory changes receded. A late trend toward declining GFR beyond 12 mo was associated with progressive glomerulosclerosis, which affected 57% of all glomeruli globally by 36 mo post-TLI. Judged by a parallel increase in volume by 59%, remaining, patent glomeruli had undergone a process of adaptive enlargement. We propose that an increasing fraction of glomeruli continues to undergo progressive sclerosis after DPLN has become quiescent, and that the prevailing GFR depends on the extent to which hypertrophied remnant glomeruli can compensate for the ensuing loss of filtration surface area.
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PMID:Outcome of the acute glomerular injury in proliferative lupus nephritis. 276 Feb 19

Lyme disease is capable of producing a wide variety of clinical pathologic conditions and lesions having in common histologic features of collagen-vascular disease. The plasma cell is an omnipotent inflammatory responder in most tissues involved by Lyme disease, ranging from relatively acute to lesions that have gone on for years. Vascular thickening also seems to be prominent, and in the dermis is accompanied by scleroderma-like collagen expansion. The disease in some ways resembles the responses seen in lupus erythematosus such as mild cerebritis with lymphocytes and plasma cells in the leptomeninges. Lymphoplasmacytic panniculitis of Lyme disease resembles lupus profundus, both in the infiltrate and the plasma cell-blood vessel relationship. The onion skin thickened vessels of the synovia resemble the vessels of lupus spleens, while the scleradermoid thickening of the dermis and various skin lesions of stage III Lyme disease suggest a collagen-vascular disorder. Finally, the perivascular lymphoid infiltrate in clinical myositis does not differ from that seen in polymyositis or dermatomyositis. All of these histologic derangements suggest immunologic damage in response to persistence of the spirochete, however few in number.
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PMID:Clinical pathologic correlations of Lyme disease by stage. 284 22

BXSB mice, a recently developed autoimmune strain, develop a human lupus-like disease with B cell hyperplasia in peripheral lymphoid organs. Unlike other experimental models of autoimmunity and human lupus, BXSB male mice manifest accelerated autoimmune phenomena through the influence of a Y chromosome-linked enhancing factor. The present studies were performed to investigate the features of B lymphopoiesis in BXSB mice and to determine whether differences exist between BXSB males and females in this respect. B lineage cell populations in the marrow of BXSB mice were identified phenotypically by studying the cytoplasmic mu-heavy chains of IgM (c mu), and functionally by their ability to acquire clonability and sIg in short-term liquid cultures. Male BXSB mice became deficient in both the precursors of functional B cells and c mu + pre-B cells by the age of 8 to 12 wk. This followed a transient increase in this population, which peaked when the mice were 2 to 4 wk old. In females, substantial numbers of functional B cell precursors and c mu + cells were maintained until more than 4 mo of age. Cells lacking Ig but bearing a B lineage cell antigen (14.8) were elevated in numbers in both BXSB males and females until 16 wk of age when compared to normal strains of mice. At the time pre-B cells and functional B precursors were elevated in numbers, some sIg- cells were shown to form colonies in mitogen-stimulated semisolid agar cultures without a period of preculture. Most of these sIg- cells seemed to bear the B lineage cell antigen (14.8). They were independent of both G-10 adherent regulatory cells and Thy-1+ cells for their colony formation. These results indicate that B lymphocyte formation may be maintained in a hyperactive state in BXSB females, whereas males become deficient in B cell precursors very early in life. This early decline might be related to the accelerated development of autoimmune disease in BXSB mice. Bone marrow transplantation studies showed that these unusual characteristics of B lymphopoiesis were reciprocally transferable with unseparated bone marrow cells between BXSB males and females. This finding indicates that sex hormones are not a critical variable in abnormal B lymphocyte formation in this strain, and that the premature deficiency of immediate B precursors in males may be regulated by a genetic factor(s) located on the Y chromosome.
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PMID:Age-dependent changes in B lymphocyte lineage cell populations of autoimmune-prone BXSB mice. 285 30


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