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)

Previously we have shown the ability to induce experimental systemic lupus erythematosus (SLE) in naive mice with pathogenic antibodies carrying the 16/6 idiotype (Id) and with the T-cell line specific for the 16/6 Id. In the present study we established and characterized a series of T-cell clones that react against diverse autoantibodies carrying the 16/6 Id and show that they are capable of inducing a SLE-like disease in mice. The T-cell clones were generated from BALB/c mice immunized with the human mAb anti-DNA antibody (SA-1) and the mouse monoclonal anti-tuberculous Ab (TB/68), both carrying the 16/6 Id. The T-cell clones proliferated only in the presence of either human or mouse mAb carrying the 16/6 Id. All the T-cell clones were found to be of the helper type (L3T4) and were H-2 restricted in their function. The injection of the clones to BALB/c mice resulted in serological findings (e.g., anti-DNA, anti-Sm), clinical manifestations (e.g., proteinuria, low white blood cell counts, increased erythrocyte sedimentation rate), and renal insult typical of SLE disease. Our data support the role attributed to pathogenic idiotypes in SLE on the one hand and that played by cellular immunity on the other. The mechanism by which Id-specific T-helper cells may induce SLE is currently not clear. The immunogenicity of the T-cell receptor (anti-16/6) and the cells themselves acting as effector/helper cells, thus leading to damage, may play a role in initiating a chain of events that ends in the production of a panoply of autoantibodies, some of which may also have a regulatory function.
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PMID:Induction of systemic lupus erythematosus in naive mice with T-cell lines specific for human anti-DNA antibody SA-1 (16/6 Id+) and for mouse tuberculosis antibody TB/68 (16/6 Id+). 183 Aug 33

The 16/6 anti-DNA idiotype (id) is a pathogenic idiotype first identified on a human hybridoma antibody derived from a patient with systemic lupus erythematosus (SLE). The SA-1 anti-DNA, which antibody was established in a similar fashion from a patient with polymyositis, also carries the 16/6 id, although it has a greater reactivity with dsDNA. The presence of the 16/6 id as defined by anti-16/6 and anti-SA-1 was determined in 3 distinct populations of patients with SLE: 502 Mexicans, 98 English (including Caucasians, West Indians, Chinese, Asians) and 93 Israelis. A similar prevalence (around 20%) of the 2 idiotypes was found, with a significant overlap. The latter finding was supported by a significant correlation noted between the prevalence of the 2 idiotypes (r = 0.58 p less than 0.001). Despite the fact that 16/6 antibody is most probably encoded by a germline gene, thus being genetically determined, no distinction in the prevalence of the ids could be detected between completely different populations of patients with SLE. This finding may support the independent pathogenic role ascribed to the 16/6 id.
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PMID:The frequency of a common anti-DNA antibody idiotype (16/6) in different populations of patients with systemic lupus erythematosus. 192 Mar 8

We have previously demonstrated the pathogenicity of the common anti-DNA idiotype designated 16/6 Id. Immunization of naive mice with the 16/6 Id induced SLE-like disease characterized by serological (e.g. anti-dsDNA and anti-Sm auto-antibodies), clinical (increased ESR, leucopenia and proteinuria), and pathological (16/6 Id deposition in kidneys) parameters. To elucidate further the role of the 16/6 Id in SLE induction the following studies were carried out: BALB/c mice were immunized with SA-1, a human anti-DNA monoclonal antibody carrying the 16/6 Id; TB-68, a mouse monoclonal anti-tuberculosis (TB) glycolipid, which binds dsDNA and carries the 16/6 Id; TB-72, a mouse monoclonal anti-TB glycolipid that binds DNA and does not harbour the 16/6 Id; and 4B4, a human anti-Sm antibody that carries the 16/6 Id. SLE was induced in BALB/c mice only when immunized with SA-1, TB-68, and 4B4, namely antibodies with diverse binding capacities albeit having the 16/6 Id. Our studies further support previous evidence on the pathogenic role attributed to the 16/6 Id in SLE, and suggest that SLE is most probably an idiotype-induced disease.
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PMID:The importance of the pathogenic 16/6 idiotype in the induction of SLE in naive mice. 240 76

A human IgM monoclonal antibody (Pol-1, SA-1) was generated by the human hybridoma technique from the peripheral blood lymphocytes (PBL) of a patient with active polymyositis. The antibody was found to bind to ssDNA, dsDNA, poly(I) and poly(G) and to carry the common lupus anti-DNA antibody idiotype (16/6 Id). Another human IgM monoclonal antibody (Pol-2, SA-2) produced by similar methods from the PBL of the same patient while in remission lacked the ligand-binding capacities of Pol-1 SA-1 and did not have the 16/6 Id. Analyses of 19 sera samples from patients with polymyositis showed no antinuclear antibodies, excluding a 40% prevalence of the 16/6 Id. The serum of the patient whose lymphocytes were employed to generate the hybridoma was negative for anti-DNA activity as well as for the 16/6 Id. This study suggests that the hybridoma technique may enable expression of dormant idiotypic affinities which do not normally appear in sera.
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PMID:A human monoclonal anti-DNA antibody derived from a patient with polymyositis having the common lupus 16/6 idiotype. 326 49