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

Naturally occurring thymocytotoxic autoantibodies (NTA) have been described in both humans and mice with SLE. To define further the role of anti-thymic autoantibodies in murine lupus, we studied the cellular and molecular specificity of a spontaneous monoclonal NTA, designated TC-17, derived from a 4-mo-old New Zealand Black mouse. TC-17, an IgM autoantibody, has been shown previously to be unreactive with Lyt-1, Lyt-2, and L3T4 (T helper) antigens. We have shown further that it is also unreactive with Thy-1. TC-17 recognizes a new thymic antigen that appears to mark a distinct subpopulation of cortisol-sensitive cortical thymocytes. The antigen consists of a single glycoprotein chain with an apparent m.w. of 88,000. TC-17 shows reduced binding to thymocytes treated with tunicamycin, indicating either that glycosylation of TC-17 antigen is necessary for TC-17 to bind to it or that glycosylation is required for expression of the antigen on the cell surface. TC-17 uniquely reacts with two of 17 murine lymphoid tumor cell lines of intermediate cellular maturity. The thymocytotoxic activity of TC-17 is absorbed by single cell suspensions of murine stomach, small intestine, large intestine, kidney, and thymus. Moreover, the specific binding of TC-17 to gut tissue of normal and germfree mice can be demonstrated by indirect immunofluorescence, suggesting antigenic cross-reactions between thymic and gut tissue. TC-17 reacts with rat thymocytes as well as it does with murine cells, indicating moderate evolutionary conservation of the TC-17 antigen. The expression of this glycoprotein by a discrete thymocyte subset may prove to be a valuable probe for the study of murine T cell differentiation.
 ...
PMID:Tissue localization and biochemical characteristics of a new thymic antigen recognized by a monoclonal thymocytotoxic autoantibody from New Zealand black mice. 392 16

The effects of total lymphoid irradiation (TLI) on serum levels of autoantibodies, and of antibodies to diphtheria toxoid, tetanus toxoid, and pneumococcal polysaccharide in patients with lupus nephritis were compared with those previously observed in rheumatoid arthritis (RA) patients. Baseline levels of antibodies to diphtheria toxoid and tetanus toxoid decreased significantly after TLI in patients with lupus and RA, but antibody levels to pneumococcal polysaccharide remained unchanged. After TLI, the levels of antinuclear and anti-DNA antibodies were reduced significantly in lupus, but levels of rheumatoid factor, antinuclear, and antigranulocyte antibodies all tended to increase in RA.
 ...
PMID:Effect of total lymphoid irradiation on levels of serum autoantibodies in systemic lupus erythematosus and in rheumatoid arthritis. 394 15

Groups of nonirradiated BDF1 mice were injected with unseparated spleen cells from B10, B10.D2, or DBA/2 donors. The diverse clinical and pathologic symptoms that developed during the course of the ensuing graft-vs-host reaction (GVHR) were related to the functional subsets of donor-T cells activated in the host. The activation of F1-specific donor T suppressor (TS) cells was confined to those GVH F1 mice that developed acute GVH disease (GVHD) (donor B10 or B10.D2). Moreover, activation in these GVH F1 mice of the Lyt-1-2+ donor TS cells sharply preceded the onset of and coincided with (week 2 to 6) the suppressive pathologic symptoms characteristic of acute GVHD, such as pancytopenia and suppression of splenic IgG production. The activation of these alloreactive TS effector cells was briefly preceded by the activation of F1-specific Lyt-1+-2- donor T helper (TH) cells and stimulation of the host's lymphoid tissue. Thus, in acute GVHD, a sequential alloactivation first of donor TH and then of TS cells was found. Those F1 mice that recovered from acute GVHD and developed stimulatory pathologic symptoms showed a concomitant loss of donor TS cell activity. An initial activation of F1-specific Lyt-1 +2- donor TH cells was also found in that parent----F1 combination (donor DBA/2), which failed to develop acute GVHD. Significantly in that combination, the alloactivation of donor TH cells was not followed by activation of significant numbers of donor TS cells. Instead, the DBA/2-injected BDF1 mice directly developed a persistent increase in splenic Ig formation and lupus-like GVHD.
 ...
PMID:Allosuppressor- and allohelper-T cells in acute and chronic graft-vs-host disease. IV. Activation of donor allosuppressor cells is confined to acute GVHD. 623 Mar 90

Neurological syndromes are prominent in systemic lupus erythematosus, but the neuropathological and mechanisms resulting in neurological dysfunction are unknown. We report a neuropathological study of the central nervous system in female NZB/W F1 mice, an animal model of systemic lupus erythematous. NZB/W mice were studied at 3, 5, 8, 12, and 14 months of age, and 36-month-old female C57B16N/NIA mice were studied as aged controls. A lymphoproliferative process was identified in the central nervous system of 39% of 8- to 12-month-old and all 14-month-old NZB/W mice. Infiltrates of lymphocytes and plasma cells were seen in subarachnoid, choroid plexus interstitial, and Virchow-Robin spaces. Lymphoid cells occasionally infiltrated brain parenchyma or accumulated as nodular masses. Concomitant visceral lymphoid infiltration was noted in 14-month-old mice. Dense deposits were seen ultrastructurally in the basal lamina of brain parenchymal capillaries of 14-month-old NZB/W mice. These dense deposits were similar in appearance to immune complexes described in glomerular basal lamina, and appeared concomitantly with an advanced lupus-like glomerulopathy. Similar deposits were not observed in choroid plexus. The possible relevance of these neuropathological changes to human central nervous system lupus is discussed.
 ...
PMID:Neuropathological features of a lupus-like disorder in autoimmune mice. 631 72

We examined the effects of two prostaglandin synthetase inhibitors, aspirin and oxaprozin, on the development of lupus-like disease in MRL/1 mice. Daily oral administration of 100 mg/kg of these compounds over a period of 3 months significantly reduced thymic lymphoid hyperplasia. In addition, aspirin but not oxaprozin significantly lowered total lymphocyte counts in the peripheral blood. Other drug-related changes, including reduced hyperplasia in the spleen and lymph nodes and an improvement in kidney vasculitis by aspirin, did not reach statistical significance. Neither aspirin nor oxaprozin influenced the circulating levels of anti-ds DNA antibodies or the severity of kidney glomerulonephritis. While the overall effects of these cyclooxygenase inhibitors were not dramatic, the results do indicate that further studies are warranted to determine the precise therapeutic role, if any, for PG-synthetase inhibitors in lupus-like disease.
 ...
PMID:Effects of oral aspirin and oxaprozin on the development of lupus-like disease in MRL/1 mice. 643 13

Weekly injection of cyclophosphamide (Cy) into MRL/Mp-lpr/lpr (MRL/l) mice, at a dose of 10-20 mg/kg, from 1 month of age prevented the development of generalized lymph node enlargement, decreased serum levels of anti-DNA antibodies and immune complexes, and markedly prolonged their life span. Cy effectively suppressed enhanced differentiation of B cells, as evidenced by decreased number of immunoglobulin secreting cells in the spleen. Cy was also shown to suppress abnormal expansion of Thy-1 positive cells in lymphoid organs of MRL/1 mice. These results suggested that Cy prevented the development of murine lupus like syndrome in MRL/1 mice through suppression of spontaneous polyclonal B cell activation and also by reducing the number of T cells to exert excessive helper activity on B cells.
 ...
PMID:Long term administration of cyclophosphamide in MRL/1 mice. I. The effects on the development of immunological abnormalities and lupus nephritis. 660 92

Three mouse strains, NZBxW, BXSB, and MRL/lpr have well documented congenital lymphoproliferative syndromes and lupus-like disease. We studied the ultrastructures of the marrows of these mice searching for a model for intramedullary lymphopoiesis. In MRL/lpr, the strain with the most severe disease, the marrow was largely populated by large lymphocytes associated with dark branching stromal cells. These stromal cells are apparently of a recently recognized cell type which has been associated with extremely accelerated eosinophilopoiesis and erythropoiesis. They did not appear in the lymph nodes and spleens of the MRL/lpr mice or in the marrows of the other strains. BXSB marrows showed some non-proliferant lymphocytic infiltrates and heightened erythropoiesis while NZBxW marrows resembled controls. We suggest that the dark stromal cells in the MRL/lpr marrows were important in supporting the production or differentiation of lymphoid precursor cells.
 ...
PMID:Ultrastructure of the bone marrow in three murine strains with non-malignant lymphoproliferative syndromes NZBxW, BXSB, and MRL/lpr. 665 Aug 75

A newly discovered autosomal recessive mutation, generalized lymphoproliferative disease (gld), in the C3H/HeJ strain of mice, determines the development of early onset massive lymphoid hyperplasia with autoimmunity. Significant lymph node enlargement is apparent as early as 12 wk of age. By 20 wk, lymph nodes are 50-fold heavier than those of coisogenic C3H/HeJ-+/+ mice. There is a concomitant increase in the numbers of peripheral blood lymphocytes. Analysis of C3H-gld lymph node lymphocyte subsets by immunofluorescence indicates an increase in numbers of B cells, T cells, and null (Thy-1-, sIg-) lymphocytes by 6-, 15-, and 33-fold compared with congeneic control mice. Serologically, gld/gld mice develop antinuclear antibodies (including anti-dsDNA), thymocyte-binding autoantibody, and hypergammaglobulinemia with major increases in several immunoglobulin isotypes. Mutant gld mice live only one-half as long as normal controls (12 and 23 mo, respectively). Interstitial pneumonitis was found in virtually all C3H-gld mice autopsied when moribund. Although immune complexes were detected in the glomerulus by immunofluorescence techniques, only 14% of the autopsied mice had significant lupus-like nephritis. Vascular disease was not found. The pattern of early onset massive lymph node enlargement, hypergammaglobulinemia, and production of antinuclear autoantibodies resembles the basic abnormal phenotype induced by the lpr (lymphoproliferation) mutation. The mutations gld and lpr are not allelic. Linkage studies indicate that gld is located between Pep-3 and Lp on chromosome 1. This new mutation adds another genetically well-defined model to the list of murine lymphoproliferative/autoimmune disorders that may be exploited to gain a clearer understanding of immunoregulatory defects and for identifying common pathogenetic factors involved in systemic autoimmune diseases.
 ...
PMID:A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. 669 32

The present study aimed to characterize and compare the inflammatory cells in the oral lesions in lichen planus and systemic lupus erythematosus. The inflammatory cell subtypes were identified by the combined use of morphological criteria and intracellular markers. In lichen planus 70-90% of all lymphocytes in a band-like submucosal infiltrate were acid alpha-naphthyl acetate esterase (= ANAE)-positive T lymphocytes. The lymphocyte band was sandwiched between mature tissue macrophages and plasma cells. In systemic lupus erythematosus (SLE) the lymphoid cell infiltrate pattern was more variable with extension of the infiltrate to the deeper connective layers and with a more patchy arrangement. The number of ANAE-negative (B) lymphocytes equalled the numbers of ANAE-positive T lymphocytes. In addition, large numbers of plasma cells were present in some lupus patients. In both diseases IgG was produced by 80% of all plasma cells in situ and there were equal portions of cells containing kappa and lambda light chains.
 ...
PMID:Oral lesions in lichen planus and systemic lupus erythematosus. A histochemical and immunohistochemical study. 675 Oct 20

BXSB mice develop a lupus-like disease characterized by B cell hyperplasia, hypergammaglobulinemia, autoantibodies, nephritis and coronary artery disease. To determine the subset of B cells responsible for disease in these mice, we bred a congenic BXSB.xid strain (greater than 99.2% inbred) with the xid gene that deletes a subset of splenic B cells. Because BXSB disease is associated with the Y chromosome, BXSB males and the autoimmune cross (NZB X BXSB)F1 males were studied. BXSB.xid males had profoundly reduced lymphoid hyperplasia, hypergammaglobulinemia, autoantibodies, renal disease, cardiac disease, and markedly prolonged survival. (NZB.xid/+ X BXSB)F1 males also demonstrated a marked protection associated with the xid gene. These studies suggest that the autoimmune disease of BXSB males is dependent upon the B cell subset deleted by xid.
 ...
PMID:The effect of the X-linked immune deficiency gene (xid) upon the Y chromosome-related disease of BXSB mice. 688 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>