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)

The immunological responsiveness of a panel of 17 patients with systemic lupus erythematosus (SLE) was studied in an in vitro model of xenogeneic sensitization against mouse lymphoid cells. Generation of cytotoxic thymus-derived (T) cells evaluated by a chromium release assay against labeled target cells was found to be drastically impaired in these lupus patients. Such depression was independent of drug therapy at the time of the study, clinical status, and other immunological parameters such as antibodies against native DNA, complement levels, cryoglobulinemia, circulating immune complexes, or T- and bone marrow-derived (B)-cell numbers. In contrast to the cytotoxic response, the proliferative responses to phytohemagglutinin, to allogeneic lymphocytes, and to xenogeneic lymphocytes were not significantly different from those of normal individuals. The latter response was shown to be H-2 restricted with the primed lymphocyte test. These results suggest the presence of a selective defect in the generation or in the expression of killer cells rather than a deficiency in antigen recognition by T cells. The role of serum factor(s) was examined by educating the lymphocytes of normal subjects in the presence of serum from SLE patients. Such manipulation affected both the generation of killer cells and the proliferative response. Finally our observations indicate that depression of cell-mediated immunity in SLE patients may be associated with several mechanisms including a cellular one, specifically affecting the generation of killer T cells, and a humoral one possibly as a result of antilymphocytic antibodies and(or) immune complexes.
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PMID:Selective depression of the xenogeneic cell-mediated lympholysis in systemic lupus erythematosus. 11 Aug 33

Criteria for the recognition of systemic lupus erythematosus (SLE) were applied to 362 subjects exposed to trichloroethylene, trichloroethane, inorganic chromium, and other chemicals in water obtained from wells in an industrially contaminated aquifer in Tucson, Arizona. Their antinuclear autoantibodies were measured by fluorescence (FANA) in serum. Ten patients with clinical SLE and/or other collagen-vascular diseases were considered separately. Results were compared to an Arizona control group, to published series, and to laboratory controls. Frequencies of each of 10 ARA symptoms were higher in exposed subjects than in any comparison group except those with clinical SLE. The number of subjects than in any comparison group except those with clinical SLE. The number of subjects with 4 or more symptoms was 2.3 times higher compared to referent women and men. FANA titers greater than 1:80 was approximately 2.3 times higher in women but equally frequent in men as in laboratory controls. ARA score and FANA rank were correlated with a coefficient (cc) of .1251, r2 = .0205 (p less than 0.036) in women and this correlation was almost statistically significant in men cc = .1282, r2 = .0253 (p less than 0.059). In control men and women neither correlation was significant. Long-term low-dose exposure to TCE and other chemicals in contaminated well water significantly increased symptoms of lupus erythematosus as perceived by the ARA score and the increased FANA titers.
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PMID:Prevalence of symptoms of systemic lupus erythematosus (SLE) and of fluorescent antinuclear antibodies associated with chronic exposure to trichloroethylene and other chemicals in well water. 174 91

The binding and functional activities of platelet-binding hybridoma autoantibodies from SLE patients were compared with those derived from normal individuals. Twenty-nine SLE-derived hybridoma antibodies and 20 normal-derived hybridoma antibodies were analyzed for binding to glutaraldehyde fixed platelets, dDNA and phospholipids, and for lupus anticoagulant activity. Twenty-four of the 29 SLE-derived antibodies and 9 of the 20 normal-derived antibodies showed one or more activities in these assays. Of the 24 SLE-derived antibodies, 8 (33.3%) were reactive in only one assay (monospecific), while the other 16 (66.7%) had more than one of these activities (polyspecific). In contrast, none (0%) of the 9 normal-derived antibodies with known activities were monospecific, while all 9 (100%) showed polyspecificity. Statistical analyses demonstrated that there was no correlation of anti-DNA activity with anti-platelet and most anti-phospholipid activities for the SLE-derived antibodies, and strong positive correlations between these reactivities for the normal-derived antibodies. Similarly, differences were observed in Western blotting analyses; SLE-derived antibodies bound more specifically to individual platelet proteins than normal-derived antibodies. Moreover, in chromium-51 release assays, all of the SLE-derived platelet-binding antibodies were cytotoxic to platelets, while none of the normal-derived platelet-binding antibodies showed significant cytotoxicity. Our results suggest that hybridoma platelet-binding autoantibodies derived from SLE patients exhibit greater antigen specificity and functional activity than similar antibodies derived from normal individuals.
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PMID:Differences between human hybridoma platelet-binding antibodies derived from systemic lupus erythematosus patients and normal individuals. 212 49

The patterns of migration of lymphoid cells from autoimmune-prone MRL-lpr/lpr, C57BL/6-lpr/lpr, MRL-+/+, and NZB mice were compared to those from sex and age-matched, normal CBA, C57BL/6, and BALB/C mice. Chromium-51-labelled spleen and lymph node cells from all autoimmune mice tested homed preferentially to the spleen relative to lymph node of the recipient strain. The data indicate that defects in lymphocyte trafficking are widespread in murine lupus and suggest a role for abnormal lymphocyte migration in the pathogenesis of this disease.
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PMID:Aberrant lymphocyte trafficking in murine systemic lupus erythematosus. 379 57

Dear Editor, Tattooing is a global and ancient practice that has endured until the present day. It was originally used to indicate religious beliefs, tribal affiliation, loyalty to a leader, or had a therapeutic function. Adverse reactions from tattooing are common, and cutaneous reactions to red pigment have been widely reported (1,2). Herein we report a case of a 30-year-old female patient admitted to our Department of Dermatology for a reaction to a tattoo localized at the violet and black areas of the tattoo on the upper part of her left leg. The patient reported that the tattoo had been made two years earlier, but the cutaneous alterations appeared after she decided to change the color from pink to violet. On physical examination, multiple erythematous nodular itching lesions were present at the areas of the tattoo in which the violet and black color were used (Figure 1). She had undergone antibiotic therapy without resolution after which topical corticosteroids were applied with temporary remission of signs and symptoms. Personal and familial medical history were negative. The patient reported a jewelry allergy that had never been investigated. Based on the suspicion of an allergic reaction we decided to execute a patch test SIDAPA series and patch test special tattoo series (copper sulfate 1% water, dimetilaminoazobenzene-p 1%, aminoazotoluene-o 1%, blue scattered 3 1%, blue scattered 124 1%, yellow scattered 3 1%, orange scattered 3 1%, red scattered 1 1%, gentian violet 2%, cadmium chloride 1% in water, nickel sulphate 5%, iron chloride 2% in water, potassium dichromate 0.5%, chromium trichloride 2%, aminoazobenzene-p 0.25%, cobalt chloride 1%, aluminum chloride 2%, titanium dioxide 0.1%, zinc 2.5%, mercury chloride 0.05% in water, kathon cg 0.01% in water, phenol 0.5%, ethylenediamine hydrochloride1%, phenylenediamine base-p 1%, formaldehyde 1% in water, phthalic anhydride 1%, rosin 20%, dibutyl phthalate 5%, hexamethylenetetramine 1%, benzophenone 5%). Both series of patch test showed positivity for nickel sulfate 5% at 48 hours (++) and 72 hours (+++). We then performed a 4 mm punch biopsy of the nodular lesions localized at the black and violet areas. The histological examination revealed dermal sclerosis characterized by inflammatory reaction with lympho-mononuclear infiltration in the perivasal zone. Macrophages with red and black pigment were present. The histological pattern was compatible with a granulomatous reaction. Tattooing can result in a wide variety of complications, whose prevalence and incidence still remain unclear. Some authors (3) classify such cutaneous complications in various ways, such as according to: - the length of their evolution: acute and chronic reactions; - the delay of onset after tattooing: early - during the healing phase - or delayed - after tattoo healing; - the type of reaction: infection, hypersensitivity reaction, etc. The practice of tattooing may have local or systemic complications. Dermatoses such as psoriasis, systemic erythematous lupus, sarcoidosis, lichen planus, and pseudo-epitheliomatous hyperplasia can be localized in the area of the tattoo, but allergic sensitivity to one of the pigments is the most frequent cause of dermatological reactions in the site of tattoo (4,5). In fact, adverse reactions to tattoo pigments, especially the red one, are well-described in literature. Furthermore, these compounds frequently contain components which are not systematically characterized. In our case, the granulomatous reaction did not correspond to an allergic reaction to the pigment. In fact, the patch test was negative for all pigments investigated, only showing a positive result for nickel sulfate. However, the specific and well-defined localization of the nodular lesions on the black and violet areas led us to hypothesize that the tattoo pigments in these areas contained some unknown component causing the reaction. In our opinion, a possible explanation could be that the new pigment that had been used contained a small amount of nickel sulfate, which caused the granulomatous reaction. In conclusion, we presented this clinical case to emphasize the widespread incidence of tattoo-related adverse effects, which are mostly caused by red pigment. Dermatologists should constantly strive familiarize themselves with current research on this practice and its complications. On the other hand, people with potential risk factors for adverse reactions should refer to a specialist before getting tattoos. Tattooists should use a checklist and informed consent to screen people with such potential risk factors. Furthermore, it is necessary to perform additional studies concerning ink and pigment components, with the aim of systemically characterizing the substances used in tattoos. Lastly, as emphasized by our case, patients at risk should referred to the dermatologist not only before getting a new tattoo but also in case of color changes in a pre-existing tattoo.
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PMID:Tridimensional Matryoshka Tattoo: An Important. 3154 68