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

It has been widely accepted that murine monoclonal antibodies against the CD 3 antigen have mitogenic effects on human T cells which mimic antigen binding via the T cell receptors. We report that T cells from patients with active systemic lupus erythematosus cannot respond to anti Leu 4 antibody, an anti CD 3 murine monoclonal antibody of the subclass IgG1. It was observed that T cells from patients with the active disease expressed as much of the Leu 4 and OKT 3 epitopes as compared to high responders, and sera from active patients could not change the expression of the Leu 4 epitope. Similarly, the low responsiveness could not be attributed to suppressor T cells, poor production of IL 2 or less expression of the IL 2 receptor. The accessory nonrosetting mononuclear leucocytes from high responders could convert the low responsiveness of these patients to high, whereas the accessory cells from active patients failed to help the responses of T cells from high responders. Likewise, exogenous IL 1 and anti Leu 4 antibody bound to Sepharose beads independently or cooperatively failed to propagate T cells from low responders. We suggest that the low response to anti Leu 4 antibody as demonstrated in the T cells of patients with active SLE may be due in part to the impairment of the secondary signals, distinct from IL 1, between helping accessory cells and responding T cells, or to the dysfunction of intracellular transmission of stimulation, and may play significant roles in the pathogenesis of SLE.
 ...
PMID:Low responsiveness to the anti Leu 4 antibody by T cells from patients with active systemic lupus erythematosus. 247 Sep 7

We have experienced a case of chronic active Epstein-Barr virus infection (CAEBV) complicated in systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS). A 35-year-old woman was admitted to our hospital with complaints of fever and dyspnea on exertion. She was diagnosed as having SLE on the basis of arthritis, oropharyngeal ulcer, lymphopenia, and positive autoantibodies against DNA, RNP and SSA. The diagnosis of APS was also made because of positive anti-cardiolipin IgG antibodies and the existence of multiple pulmonary infarction with pulmonary hypertension. The administration of 30 mg/day of prednisolone and anti-coagulation significantly improved clinical symptoms. However, she was again admitted to the hospital four months later because of progressive liver damage and pancytopenia. Increment of prednisolone did not improve the clinical situation and she expired because of pulmonary hemorrhage. At autopsy, there were a significant increase of histiocytes with hemophagocytosis and a dense infiltration of atypical lymphocytes in the liver, spleen, lymph nodes and bone marrow. Infiltrated lymphocytes were positive for CD 3 and EBER 1 in immunohistochemical staining and EBVmRNA was detected by in situ hybridization. Final pathological diagnosis was CAEBV with hemophagocytic syndrome in association with lupus nephritis, pulmonary hemorrhage and pulmonary infarction.
 ...
PMID:[An autopsied case of chronic active Epstein-Barr virus infection complicated in systemic lupus erythematosus and antiphospholipid antibody syndrome]. 1259 14