Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

C3-bearing immune complexes and C3 activation products were detected by using two monoclonal antibodies, one specific for a neoantigenic determinant on C3c and the other for C3d. To quantitate immune complexes, the anti-C3c or anti-C3d antibodies were fixed to microtiter plates and reacted with test plasma. The binding of C3-bearing immune complexes in this plasma was then measured with radioisotope- or enzyme-labeled anti-human IgG. To test for C3 breakdown products, solid-phase monoclonal antibody to the C3d neoantigen was reacted with EDTA-plasma samples, and fixed iC3b or C3d was measured with a polyclonal anti-C3 antibody. Patients with autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Sjogren's syndrome, and paracoccidioidomycosis were found to contain immune complexes bearing C3b/iC3b or C3d. In most conditions, there were more C3d-containing immune complexes than C3b/iC3b. Although CR1 (C3b receptors) rapidly converted immune complex-bound iC3b to C3dg/C3d and lupus patients had reduced CR1, no correlation between the state of C3 on circulating immune complexes or levels of immune complexes and CR1 numbers was seen. However, levels of C3-fixing ICs correlated with levels of C3 activation products. This assay system with monoclonal antibodies to neoantigens expressed on activated, but not native, C3 provides sensitive and specific means for detecting and classifying C3-fixing immune complexes and for assessing C3 activation.
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PMID:Monoclonal antibodies against complement 3 neoantigens for detection of immune complexes and complement activation. Relationship between immune complex levels, state of C3, and numbers of receptors for C3b. 293 66

Retro-inverso peptides which contain NH-CO bonds instead of CO-NH peptide bonds are much more resistant to proteolysis than L-peptides. Moreover, they have been shown recently to be able to mimic natural L-peptides with respect to poly- and monoclonal antibodies (Guichard, G., Benkirane, N., Zeder-Lutz, G., Van Regenmortel, M. H. V., Briand, J. P., and Muller, S. (1994b) Proc. Natl. Acad. Sci. U.S.A. 91, 9765-9769). We have further tested the capacity of retro-inverso peptidomimetics to serve as possible targets for antibodies produced by lupus mice and by patients with rheumatic autoimmune diseases. Several retro-inverso peptides corresponding to sequences known to be recognized by autoantibodies were synthesized, namely peptides 28-45 and 130-135 of H3, 277-291 of the Ro/SSA 52-kDa protein, and 304-324 of the Ro/SSA 60-kDa protein, and tested with autoimmune sera by enzyme-linked immunosorbent assay. We have found that retro-inverso peptides are recognized as well as or even better than natural peptides by antibodies from autoimmune patients and lupus mice. This new approach may lead to important progress in the future development of immunodiagnostic assays, particularly in the case of diseases characterized by inflammatory reactions in the course of which the level of degradative enzymes is increased.
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PMID:Retro-inverso peptidomimetics as new immunological probes. Validation and application to the detection of antibodies in rheumatic diseases. 765 48

We have previously described a novel complex of proteins which contains the U1snRNP-A protein (U1A) but no other small nuclear ribonucleoprotein particle (snRNP) components (O'Connor et al., RNA 1997;3:1444-55). Antibodies to this novel complex inhibit both splicing and polyadenylation in vitro of a test pre-mRNA (O'Connor et al., RNA 1997;3:1444-55; Lutz et al., RNA 1998;4:1493-9). This novel complex of proteins was identified using an unusual mouse monoclonal antibody (MoAb), called MAb 12E12. We were interested to know if autoimmune patient sera were similar to this MoAb. We have discovered a novel specificity of systemic lupus erythematosus patient sera reminiscent of MAb 12E12 in that the patient serum, like 12E12, (1) does not recognize U1A when bound to U1 RNA, (2) recognizes primarily the epitopes in the amino-terminal third of the protein, including RNA recognition motif 1 (RRM1) and (3) inhibits in vitro polyadenylation. These findings may lead to the discovery of previously undescribed autoantigens as components of the novel protein complex, and may provide insight into autoimmune diseases.
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PMID:Novel specificity of anti-U1A autoimmune patient sera. 1254 1

We developed and analyzed an Enzyme-Linked Immunosorbent Assay (ELISA) in order to detect antibodies in sera from sporotrichosis patients. We used a crude antigen of Sporothrix schenckii sensu stricto, obtained from the mycelial phase of the fungi. Positive sera were analyzed by other serological techniques such as double immunodiffusion (IGG) and counterimmunoelectrophoresis (CIE). The assay was validated by using sera from patients with other pathologies such as: histoplasmosis, paracoccidioidomycosis, tuberculosis, leishmaniasis, lupus and healthy individuals as negative controls. For the Sporothrix schenckii sensu stricto antigen, we found a 100% of specificity by every technique and sensitivity higher than 98% with IDD, CIE and ELISA. Our results show a high sensitivity and specificity for the Sporothrix schenckii sensu stricto antigen, so it can be used for IDD, CIE and ELISA. The results suggest that this antigen could be used in conjunction with other conventional tests for differential diagnosis and may be useful for monitoring the disease progression and response to treatment.
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PMID:[Serological diagnosis of sporotrichosis using an antigen of Sporothrix schenckii sensu stricto mycelium]. 2629 53

Paracoccidioidomycosis (PCM) is a systemic disease caused by the dimorphic fungus Paracocdioides brasiliensis. The infection primarily reaches the lungs by the inhalation of fungi spores and later can disseminate to other organs causing secondary oral lesions. Systemic lupus erythematosus (SLE), on the other hand, is an autoimmune chronic inflammatory disease that affects various organ systems, including skin and oral cavity. Here we report a 39-year-old female patient bearing SLE and presenting an ulcerated lesion on the hard palate extending to the superior alveolar ridge, diagnosed as PCM. Itraconazole 200mg was prescribed and photodynamic therapy (PDT) was also instituted in a way to help dealing with the PCM infection while assisting such an immunocompromised patient to heal. PDT consisted of topically placing toluidine blue dye at 37.5mg/L for 5min, followed by low-level laser irradiation (660nm; 100J/cm2; 40mW of power; 100s per point). Forty days after beginning the treatment, the patient showed total regression of the oral lesion and absence of painful symptoms. The serologic test was performed again after six months of therapy and was negative; the patient continues to be followed periodically.
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PMID:Photodynamic inactivation of oral paracoccidioidomycosis affecting woman with systemic lupus erythematosus: An unusual case report. 2801 7