Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0409974 (
lupus
)
22,386
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Those caring for children should recognize that cutaneous findings are common in children with host defense defects. Atopic dermatitis, recurrent or persistent pyodermas, candidiasis and
lupus
-like syndromes, should signal the possibility of host defense deficiencies. Particularly the findings of atopic dermatitis and recurrent skin abscesses should alert the clinician to determine serum
IgE
levels and neutrophil chemotaxis in such patients. The triad of generalized seborrheic dermatitis, failure to thrive, and diarrhea in an infant should bring to mind Leiner disease or severe combined immunodeficiency disease.
...
PMID:Cutaneous manifestations of defective host defenses. 32 7
A patient with hypocomplementemic urticarial vasculitic syndrome (HUV) is presented. This is an immunological pathology, limited to skin or multisystemic, that requires a differential diagnosis with erythematosus systemic
lupus
on the same occasions. The ever-present symptom is skin participation, such as urticaria-angioedema or fixed exanthema; biopsy shows necrotizing venulitis with polymorphonuclear infiltration and leukocytoclastic powder. Typical laboratory data are: diminished C3, C4 and C1q; C1 inhibition can be low or normal; the more characteristic finding is the presence of C1q associated immunocomplexes. Leukocytoclastic necrotizing vasculitis was found in the skin biopsy. During the course of illness (three years) the patient presented moderate cutaneous symptoms and asthma, without other systemic participation. During this period, antihistamines and, occasionally, corticoids were administered with improvement. Moreover, the patient presented urticaria related to ampicillin ingestion, and furthermore, the presence of anaphylaxis to beta-lactam was diagnosed in vivo and specific
IgE
was found in the laboratory study. This feature was previously observed by other authors; however, we cannot determine why the
IgE
-mediated allergy to beta-lactam and a complement pathology like HUV are related.
...
PMID:Hypocomplementemic urticarial vasculitic syndrome, asthma and anaphylactic reaction with ampicillin. 166 67
The role of IL-4 in the cellular interactions leading to the induction of CTL tolerance to H-2b alloantigens and to the development of a
lupus
-like autoimmune disease in BALB/c mice after neonatal injection with (C57BL/6 x BALB/c)F1 cells was investigated in vivo by using an anti-IL-4 mAb. Treatment of F1 cell-injected BALB/c mice with 15 mg of anti-IL-4 mAb was shown to interfere with tolerance induction, as assessed by the high percentages of H-2b target cell lysis and the very low or undetectable levels of B cell chimerism markers observed in these mice. Treatment with 4.5 mg of anti-IL-4 mAb interfered with tolerance induction only in one-third of F1 cell-injected BALB/c mice, but that dose induces specific modulations of the autoimmune manifestations in all mice, leading to the nearly complete prevention of the disease. In particular, the production of anti-ssDNA IgG1 and of total IgG1 and
IgE
antibodies was seriously affected by the treatment, as well as the proliferation and membrane Ia and K expression of F1 donor splenic cells and thymic APC. Treatment of F1 cell-injected BALB/c mice between 24 and 48 h of life with 0.5 mg of anti-IL-4 mAb did not interfere with tolerance induction, but had similar effects on the autoimmune syndrome as treatment with 4.5 mg. These results suggest that, after F1 cell injection of newborn mice, IL-4 plays an important role in the cellular interactions leading to the induction of tolerance to the corresponding alloantigens and to the development of the associated autoimmune syndrome.
...
PMID:In vivo effects of anti-IL-4 monoclonal antibody on neonatal induction of tolerance and on an associated autoimmune syndrome. 221 49
We have developed a model of
IgE
-dependent, mast cell-mediated arthritis in rats. One knee joint (test joint) of a Sprague-Dawley rat was injected with 1 micrograms of a monoclonal
IgE
specific for dinitrophenol, and the contralateral (control) joint was injected with the same amount of an irrelevant monoclonal
IgE
in phosphate buffered saline or with phosphate buffered saline alone. Within 5 minutes of intravenous injection of antigen, an acute, transient arthritis occurred in the test joints only, with swelling and extravasation of intravascular blue dye and 125I-labeled albumin, decreased numbers of stainable mast cells, and decreased histamine content of the joint synovium. Pretreatment of experimental animals with H1 and H2 antihistamines did not completely block the reaction. These data show that
IgE
-dependent synovial mast cell degranulation causes a transient, nondestructive arthritis, reminiscent of
lupus
arthritis and intermittent hydrarthrosis.
...
PMID:Demonstration and characterization of a transient arthritis in rats following sensitization of synovial mast cells with antigen-specific IgE and parenteral challenge with specific antigen. 245 75
Systemic lupus erythematosus was diagnosed in a dog with concurrent nematode infection. The clinical signs of disease were unusually severe and included multiple neurologic deficits, polyarthritis, and weight loss. The dog was thrombocytopenic, and serotest results included positive
lupus erythematosus
test, positive rheumatoid factor test, positive antinuclear antibody test, hypergammaglobulinemia, and high platelet-associated IgG concentration. After treatment of hookworm, whipworm, and heartworm infections concurrently with corticosteroid and empiric treatment, the dog's condition improved. However, 10 days later, cyclophosphamide administration was necessary for continued immunosuppression. The dog was euthanatized because of progressive deterioration and development of canine coronavirus diarrhea. Serotest data generated from the dog's serum obtained at the time of referral suggested that autoantibodies and circulating immune complexes may have included
IgE
isotypes.
...
PMID:Systemic autoimmune disease and concurrent nematode infection in a dog. 255 67
The prevalence of naturally occurring anti-
IgE
autoantibodies was assessed by surveying 387 sera from atopic, nonatopic, and autoimmune patients. A significant number of children (28.5%) and adults (20%) with no history of allergy had high levels of autoanti-
IgE
. The level of autoantibodies to
IgE
in children with clinical asthma or atopic eczema was not significantly elevated over normal. Similarly, adults with atopic asthma, allergic rhinitis, or urticaria or sera from individuals with rheumatoid arthritis or systemic
lupus
erythromatosis showed no significant elevation of auto-anti-
IgE
. In contrast, 82% of adults with eczema had medium to high levels of auto-anti-
IgE
and the mean concentration in sera was significantly (P less than 0.01) raised. The relevance of auto-anti-
IgE
in atopic eczema is discussed.
...
PMID:A survey of nonatopic and atopic children and adults for the presence of anti-IgE autoantibodies. 278 44
In 1979, suspicion of convulsive disorder was diagnosed in a 9-year-old girl, who consequently underwent treatment with carbamazepine. In 1983, she developed hyperimmunoglobulinemia E syndrome.
IgE
values reached up to 5,400 u/ml. During the following weeks, we detected systemic lupus erythematosus with epimembranous glomerulonephritis histologically proved. The patient's immunological status does not allow the decision whether the
lupus erythematosus
may be classified as idiopathic or as a drug-induced disease having started with the convulsive disorder. Discontinuation of the carbamazepine therapy will not give a further hint on the etiology of the
lupus erythematosus
since long-lasting anticonvulsive therapy using this drug leads to an irreversible course of the disease.
...
PMID:[Systemic lupus erythematosus and hyper-IgE syndrome in a 13-year-old child]. 294 Jul 60
Antibody dependent cellular cytotoxicity (ADCC) is a recently described mechanism of immunologic lysis in which cellular targets sensitized by specific antibodies are efficiently and selectively lysed by Fc receptor (FcR) bearing nonspecific effectors. Immunoglobulins of various classes (IgG, IgM, IgA,
IgE
) and various cellular effectors (large granular lymphocytes, monocyte/macrophages, T lymphocytes, neutrophils, and eosinophils) can induce ADCC in vitro, and the importance of ADCC in vivo is being tested experimentally in resistance to viral, bacterial, and parasitic infection, in tumor surveillance, in allograft rejection, and in inflammatory diseases. There is much indirect evidence that ADCC may be the mechanism of damage of different cellular targets in skin diseases, but the best direct evidence concerns immunologic keratinocyte damage, especially in cutaneous
lupus erythematosus
(LE). We have shown that keratinocytes of several species are highly susceptible to lymphocyte and monocyte-mediated ADCC, but not to neutrophil or eosinophil ADCC in vitro using two different cytotoxicity assays. In contrast, complement was a relatively ineffective mediator of lysis of metabolically intact keratinocyte targets. Patients with certain cutaneous
lupus
syndromes have serum antibodies capable of inducing monocyte and lymphocyte ADCC of targets coated with extractable nuclear antigens. We have shown that these antigens apparently move to the cell membrane of keratinocytes in vitro following ultraviolet irradiation. In an animal model, we have shown that antibodies to SSA/Ro bind to human keratinocytes in vivo, especially after ultraviolet irradiation. This antigen/antibody system is highly associated with 3 different photosensitive LE syndromes. The experimental linkage of UV radiation to autoantibody binding to keratinocytes and the demonstration of mononuclear cell-mediated ADCC causing keratinocyte lysis support our hypothesis that the keratinocyte damage and mononuclear cell infiltrate seen histologically in cutaneous LE are part of an ADCC process.
...
PMID:Antibody-dependent cellular cytotoxicity and skin disease. 387 44
The ability of basophils and tissue mastocytes activated by sensitised
IgE
antibodies to release mediators in the presence of the specific antigen underlies immediate hypersensitivity reactions. This phenomenon can be explored by the in vitro basophil degranulation test adopted not only in experimental pathology, but in human allergological pathology and in the study of post-streptococcal and
lupus
glomerulonephritis. The test has been carried out to analyse sensitisation to iodate contrast media in 71 patients already submitted to contrastography, 37 of whom had given evidence of allergic reactions. All patients with a previous history of sensitisation presented, in vitro, a positive reaction (56 + 15.3% degranulation) in the presence of the contrast medium. Against this, none of the patients with negative test presented an allergic reaction during contrastography. Stress is laid on the practical importance of the test prior to performance of contrastography so as to predict possible sensitisation and select the most suitable medium.
...
PMID:[The value of the basophil degranulation test on the study of hypersensitivity reactions to iodinated contrast media]. 616
Fifty randomly selected asthmatic patients were studied. In each the sex, age, time of onset of symptomatology, symptomatologic score (from 0 to 3), blood eosinophilia,
IgE
by the PRIST method and Tart cells in blood (investigated by the same method as is used in the search of LE cells in collagen diseases) were considered. Tart cells were recognized as in Miale Haemotology (9) as monocytes and occasionally polymophonuclar leucocytes with one or two round inclusions in their protoplasm owing to the phagocytosis of leukocyte nuclei. In contrast with LE cells, these inclusions are not homogeneous contain chromatin and nuclear membrane material and often have a dark ring of hyperchromic material. We have found that these cells can not be evoked passively by application of patient serum to normal leukocytes. In no case of positive Tart cells was antinuclear serum factor found by immunofluorescence as seen in
lupus
erythematous disease. 33 per cent of the 50 asthmatic patients tested had Tart cells in their blood. They were very scarce, only one or two in four Wright stained smears. This fact is probably why these cells were not recognized before. The positive Tart cell group was on the average the same age as the negative group. On the other hand, in the positive Tart cell group the proportion of men with respect to women, the time span from the onset of asthmatic symptoms (p less than 0,05), the symptomatology score (p less than 0,005) and blood eosinophilia (p less than 0,005) were increased. In contrast
IgE
was decreased on the average (p less than 0,05).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Finding of Tart cells in asthmatic patients. Relation to IgE and other parameters]. 620 75
1
2
3
4
5
Next >>