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)

Chromosome aberrations such as gaps and breaks of one or both chromatids, acentric fragments, dicentrics, ring chromosomes and other abnormal chromosomes are observed in lymphocyte and fibroblast cultures as well as in direct bone marrow preparations from patients with systemic sclerosis. A serum factor producing chromosome breaks in mitoses from healthy donors was observed in 37 of 42 scleroderma patients. The biochemical nature of this breakage factor is still undefined. Increased breakage is also noted in a high percentage of healthy family members of scleroderma patients. It is also a common feature of related disorders such as lupus erythematosus, dermatomyositis, periarteritis nodosa and rheumatoid arthritis. An increase in chromosome breaks and rearrangements is also present in NZB mice developing spontaneously an autoimmune disorder that has been extensively studied by workers interested in lupus erythematosus. The similarity of the cytogenetic findings provides the opportunity to use these mice as an experimental model to investigate relationships between immunological perturbations and chromosomal aberrations.
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PMID:Chromosomal breakage in systemic sclerosis and related disorders. 1 37

Measurements of transcobalamin II (T.C. II) concentrations in 26 patients with lupus erythematosus, 4 with dermatomyositis, 2 with autoimmune haemolytic anaemia, and in 40 immunosuppressed renal-transplant patients showed that T.C. II levels were raised during active phases of autoimmune disease. Changes in T.C. II levels correlated better with the clinical course of autoimmune disease than did changes in C3, the titre of antinuclear antibody, or native D.N.A.-binding capacity.
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PMID:Increased unsaturated transcobalamin II in active autoimmune disease. 7 32

In 4 women lymphomas developed 2 months to 12 years after the onset of systemic lupus erythematosus. An association between the two diseases had previously been reported in 14 cases, in 6 of which the lymphoma either preceded or was diagnosed at the same time as the autoimmune disease. In systemic lupus erythematous early biopsy of suspect lymph-nodes is recommended.
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PMID:Systemic lupus erythematosus and lymphoma. 8 Jun 83

Eleven patients were studied while taking the beta blocker acebutolol for a period ranging from 12 to more than 24 wk. Control titers for fluorescent antinuclear antibody (ANA) were obtained in all. Serial testing was performed over the duration of the therapy and following its discontinuation. Additional immunologic testing was performed in most patients. The patients were observed closely for the development of clinical autoimmune disease. Using a sensitive assay, fluorescent ANA developed in 8 of 9 patients with negative values in the control period. In no patient has evidence of clinical autoimmune disease developed. In general, the titers of ANA tended to rise with increasing duration of therapy and decline after its discontinuation. Positive lupus erythematosus cell preparations were also observed in several patients. These data suggest that autoantibodies are frequently induced by acebutolol and, although no evidence of clinical autoimmune disease has been reported, immunologic surveillance is warranted.
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PMID:Development of antinuclear antibodies during acebutolol therapy. 8 91

The age-dependent capacity of NZB and (NZB x NZW)F1 hybrid, BALB/c, DBA/2, C57BL/6 and C3H mice to generate T cell-mediated immune responses was assessed qualitatively and quantitatively by measuring the following effector functions: (a) the time course of alloreactive cytotoxic T-cell activity triggered in vitro was comparable for NZ and other mouse strains; cell reactivity generated in vivo against EL4 tumour cells was low in young (NZB x NZW)F1 mice and in DBA/2 mice but was comparable for older (NZB x NZW)F1, NZB and other mouse strains; (b) the time-dependent, vaccinia virus-specific, cytotoxic T-cell activity after systemic infection was similar for all mouse strains; (c) the T cell-dependent primary footpad swelling after local injection with lymphocytic choriomeningitis virus was within the same range for all mouse strains tested with respect to size and kinetics of the reaction; (d) the cell-mediated immune protection against Listeria monocytogenes after systemic infection revealed that NZ mice are, independent of age, more susceptible than C3H or C57BL/6 mice and comparable to A strain mice. Therefore, these responses in young, or clinically relatively normal older, NZB or (NZB x NZW)F1 strains that are affected by a lupus-like autoimmune disease did not differ markedly from the range of responses of other mouse strains of 2-14 months of age, which are not known to be similarly diseased. Thus, overall cell-mediated immunity of NZ mice as assessed quantitatively and kinetically in these functional models is within normal ranges. Possible T-cell defects may therefore be selective and either do not occur or were not detected in these models.
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PMID:Comparison of T cell-mediated immune responsiveness of NZB, (NZB x &NZW)F1 hybrid and other murine strains. 14 94

Reagents and equipment are now readily available to make fluorescent antibody techniques routine diagnostic procedures. Antinuclear antibodies are detectable by such methods and are useful in the diagnosis of autoimmune disease. By defining not only the site of tissue damage but also the specific components deposted at that site, immunofluorescence applied to renal biopsies has helped to elucidate the nature of otherwise similar appearing processes. Fluorescent techniques also facilitate diagnosis of such skin diseases as lupus, bullous pemphigoid and pemphigus.
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PMID:Diagnostic applications of the fluorescent antibody method. 17 15

Strain BXSB/Mp mice develop a spontaneous lupus-like syndrome which is strikingly accelerated in males. The accelerated autoimmune disease occurs in male F1 hybrids with strains NZB/BINJ, SJL/J, and C57BL/6J when the male parent is BXSB but not in the reciprocal hybrid male nor in females. The pattern is similar in F2 hybrids with strains NZB and SJL. The accelerated disease in males occurs only when the Y chromosome is derived from recombinant inbred strain BXSB and ultimately from strain SB/Le.
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PMID:A Y chromosome associated factor in strain BXSB producing accelerated autoimmunity and lymphoproliferation. 31 77

Early in life, mice of four kinds [NZB, (NZB X NZW)F1, MRL/1, and male BXSB] with autoimmune disease spontaneously produced far more (greater than 3 S.D.) anti-hapten antibody-forming cells in spleens and greater concentrations of anti-hapten antibodies in sera than immunologically normal strains of mice (AKR, BALB/c, C57BL/6, DBA/1-J, DBA/2J, LG/J, 129, NZW, and female BXSB). This increased nonspecific antibody production by the abnormal animals' B cells correlated well with the spontaneous development of anti-single-stranded DNA antibodies, but not with serum levels of the viral envelope glycoprotein, gp70. These results suggest that the spontaneous formation of autoantibodies in mice whose immunologic disorder is manifested by a lupus-like disease may result from polyclonal activation of B cells by endogenous or exogenous B cell activators.
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PMID:Increased spontaneous polyclonal activation of B lymphocytes in mice with spontaneous autoimmune disease. 36 41

Spleen cells from normal mice were cultured with Concanavalin A to produce an immunosuppressive supernate. This supernate was used to treat the lupus-like autoimmune disease of NZB/NZW mice. Such treated mice lived significantly longer than did controls, but only if treatment was initiated early in the course of the illness.
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PMID:Therapeutic studies in NZB/NZW mice. VI. Age-dependent effects of concanavalin A stimulated spleen cell supernate. 63 86

Transcobalamin II (TC II) is a serum protein responsible for transporting vitamin B12 to the cells. A previous observation of a child with congenital TC II deficiency and agammaglobulinemia suggested that this protein plays an important role in the immune response. Accordingly, TC II levels ere determined in 32 patients with autoimmune disease (AID) (i.e. 26 with lupus erythematosus, 4 with dermatomyositis, and 2 with autoimmune hemolytic anemia) and in 40 patients with acquired immunodeficiency due to chemotherapy. It was found that elevated TC II levels corresponded to active phases of AID. Changes in TC II levels correlated better with the clinical course of AID than complement, antinuclear antibody or native DNA binding capacity. This suggests that TC II could be a valuable parameter in following up activity of AID.
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PMID:[Increase of unsaturated transcobalamine II in autoimmune diseases; effect of immunosuppressive therapy (proceedings)]. 69 99


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