[Recent developments in high-dose immunoglobulin therapy: therapeutic plasma exchange, autoimmune diseases].
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Anti-Glomerular Basement Membrane Disease↗
Biomedical subjects
F Krapf
Publications and source records attributed to F Krapf.
Studies on the specificity of in vitro induced lymphocytotoxicity to SV40-transformed fibroblasts.
Cytotoxic effector lymphocytes were induced by in vitro immunization of lymph node and spleen cells from AKR-mice (H-2k) and from BALB/c-mice (H-2d) to syngeneic SV40-transformed fibroblasts. The T cell-dependent cytotoxicity was specific for target cells expressing the same H2-specificity as the immunizing cells. Nontransformed fibroblasts as stimulator cells did not induce efficient cytotoxicity to transformed or nontransformed target cells. Incubation with phytohemagglutinin during the sensitization period modified the specificity of the T cell-mediated lysis of syngeneic SV40-transformed fibroblasts: allogeneic as well as syngeneic target cells were destroyed by these effector cells. However, the polyclonal stimulant activates preferentially cytotoxicity to H2-matched target cells. The in vitro generation of cytotoxic effector cells was restricted to living SV40-transformed fibroblasts as immunizing cells; it was not possible to immunize lymphocytes in the presence of membrane proteins prepared from the SV40-transformed cells. The cytotoxicity of the in vitro immunized lymphocytes was inhibited by incubation with membrane protein preparations from syngeneic or allogeneic SV40-transformed fibroblasts.
Animals↗
[Plasma nucleic acids and their possible pathophysiologic significance in systemic lupus erythematosus].
The discussion of the possible pathophysiological role of plasma and/or serum nucleic acids from patients suffering from systemic lupus erythematosus is nearly identical with the still unsolved question regarding the antigen, i.e., the possible autoantigen-inducing antibodies against native double-strand DNA (dsDNA). This question is of special interest, since native dsDNA per se is not immunogenic. As repeatedly demonstrated, circulating antibodies of the isotype IgG against dsDNA can be correlated with the disease activity and, particularly, with renal involvement. Antibodies against native dsDNA were isolated from affected organs from SLE patients. The analysis of circulating immune complexes revealed dsDNA, as well as antibodies against dsDNA as complex components. DNA-anti-dsDNA serum immune complexes could also be demonstrated in patients with a so-called seronegative SLE, i.e., in patients not showing any free antibodies against native dsDNA in their sera. Furthermore, the involvement of antibodies against native dsDNA in pathogenic mechanisms of SLE patients becomes particularly evident from animal models. Regarding the induction of dsDNA antibodies, it is of special interest that in animal models such as the MLR/lpr mouse, anti-dsDNA antibodies are rather antigen-selected than they are a consequence of a "random" polyclonal B cell stimulation. Likewise, by the demonstration of somatic mutations of clonal human IgG-anti-dsDNA antibodies from SLE patients it has recently been possible to prove that these autoantibodies are also most probably antigen-selected.(ABSTRACT TRUNCATED AT 250 WORDS)
Autoantibodies↗
The estimation of circulating immune complexes, C3d, and anti-ds-DNA-antibody serum levels in the monitoring of therapeutic plasmapheresis in a patient with systemic lupus erythematosus. A case report.
A short-time monitoring of therapeutic plasmapheresis in a patient with systemic lupus erythematosus (SLE) by the estimation of circulating immune complexes, C3d serum levels and anti-ds-DNA-antibodies is described. It was found that serum immune complexes, C3d, and anti-DNA-antibodies decreased even further shortly after plasma exchange. The decrease found in C1q binding material in the patient's serum was paralleled by a decrease in serum immune complexes containing acridine orange binding material, possibly representing ds-DNA. A rapid increase of serum immune complexes, C3d, and anti-ds-DNA-antibodies after plasma exchange therapy indicated an antibody rebound phenomenon followed by a relapse of the disease.
Adult↗