Isotype and cytotoxicity spectra of anti-lymphocyte antibodies in patients with systemic lupus erythematosus

Edwards, Bruce S.; Searles, Robert P.; Brożek, Celestyn M.; Richards, Robyn; Savage, Susan; Nolla, Hector; Hoffman, Charles L.

doi:10.1016/0090-1229(87)90086-9

Cited by 8 publications

(4 citation statements)

References 43 publications

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“…ADCC was measured by an autologous peripheral blood lymphocyte assay as described by Edwards et al (1987). The cytotoxicity of NK cell populations was determined by a 51Cr release assay as described above, except that autologous cells from the same donor as the effector cells were incubated with serum from lupus erythematosus patients and used as targets.…”

Section: Antibody Dependent Cellular Cytotoxicitymentioning

confidence: 99%

“…The cytotoxicity of NK cell populations was determined by a 51Cr release assay as described above, except that autologous cells from the same donor as the effector cells were incubated with serum from lupus erythematosus patients and used as targets. Circulating anti-lymphocyte antibodies are a common occurrence in patients with systemic lupus erythematosus (Edwards et al, 1987). Autologous cells incubated with phosphate-buffered saline (PBS), pH 7.2, served as negative controls.…”

Section: Antibody Dependent Cellular Cytotoxicitymentioning

confidence: 99%

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Reversal of lovastatin‐mediated inhibition of natural killer cell cytotoxicity by interleukin 2

Cutts

Bankhurst

1990

Journal Cellular Physiology

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The activation of human natural killer (NK) cell cytotoxicity by interleukin 2 (IL-2) is well established, although the biochemical mechanisms of this stimulation have not yet been fully delineated. Earlier, we reported that treatment of NK cells with an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase such as compactin or lovastatin significantly abrogates the in vitro killing of a susceptible human erythroleukemic cell line and that this inhibition can be completely reversed by 2 hr of exposure to mevalonate (J. Cell. Physiology 139:550-557, 1989). We report here that 24 hr of treatment with IL-2 also reverses lovastatin inhibition of NK cell function. In addition to natural cytotoxicity, IL-2 also restores chemotactic and antibody dependent cellular cytotoxicity functions to lovastatin-treated cells. IL-2 does not stimulate proliferation of these cells during this time period, nor does it affect the phenotypic composition of the NK cell preparations. Although IL-2 was able to reverse the lovastatin-mediated inhibition of every cell function we examined, it had no effect on the inhibition of cholesterol biosynthesis as measured by [3H]acetate incorporation into non-saponifiable lipids, nor did it stimulate HMG CoA reductase activity. These findings support the hypothesis that there is a non-sterol isoprenoid product which is required for NK cell cytotoxicity and chemotaxis. In addition, the data suggest that IL-2 stimulation of NK cells proceeds by an isoprenoid-independent pathway.

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Section: Antibody Dependent Cellular Cytotoxicitymentioning

confidence: 99%

Section: Antibody Dependent Cellular Cytotoxicitymentioning

confidence: 99%

Reversal of lovastatin‐mediated inhibition of natural killer cell cytotoxicity by interleukin 2

Cutts

Bankhurst

1990

Journal Cellular Physiology

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“…Anti‐dsDNA antibodies have been associated with kidney pathology 4, anti‐Ro and anti‐La responses with neonatal lupus and congenital heart block 5, and anti‐phospholipid antibodies with recurrent spontaneous abortion 6. Additionally, titers of complement‐fixing antibodies to cell‐surface moieties upon leucocytes are negatively correlated with circulating leucocyte numbers 7. While some studies indicate a correlation between anti‐ribosomal P antibodies and neuropsychiatric manifestations 8, contradictory data have also emerged.…”

Section: Introductionmentioning

confidence: 99%

Endogenous humoral autoreactive immune responses to apoptotic cells: Effects on phagocytic uptake, chemotactic migration and antigenic spread

et al. 2008

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Enhanced cell death and deficient clearance of cellular debris are thought to contribute to increased self-antigen exposure in systemic autoimmune disease. To investigate the characteristics of early humoral autoimmune responses, six monoclonal antibodies were generated from two autoimmune prone strains of mice. All antibodies specifically bound the surface of late-stage apoptotic cells. Similar antibody reactivities were present in the sera of patients with systemic lupus erythematosus. While IgM antibodies significantly reduced the phagocytic uptake of apoptotic thymocytes, IgG antibodies enhanced uptake. Poly-reactivity was demonstrated in the recognition of ribonucleoproteins and lipids. An antibody reactive towards lysophosphatidylcholine reversed lysophosphatidylcholinemediated inhibition of LPS-induced TNF-a production and adversely affected the transmigration of phagocytes towards an apoptotic stimulus. In several instances, CDR were characterized by the accumulation of somatic mutations. Anti-idiotypic antibodies generated upon immunization bound distinct cellular moieties and self-antigens. Polyspecific, apoptotic cell-reactive autoantibodies can therefore directly impact upon the course of disease by influencing phagocytic uptake of apoptotic cells, by inducing a proinflammatory environment through neutralization of bioactive lipids, by blinding phagocytes to the presence of dying cells through the negation of lipidic chemotactic signals, and by mediating diversification of the humoral autoimmune response via the idiotypic network.

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“…However, circulating anti-HLA-DR antibodies (IgM isotype) were seen after immunization with tetanus in normal volunteers (25). Anti-HLA-DR antibodies have also been described in patients with rheumatoid arthritis, systemic lupus erythematosus (SLE), and Hodgkin disease (26)(27)(28). The immunoglobulin fraction of sera derived from patients with SLE decreased antigen presentation by macrophages and was correlated with the presence of anti-lymphocyte antibodies (29).…”

Section: Recognition Of Uas Heterodimers By the Anti-ia1f 18-mermentioning

confidence: 99%

A synthetic peptide from the third hypervariable region of major histocompatibility complex class II beta chain as a vaccine for treatment of experimental autoimmune encephalomyelitis.

Topham

Nag

Arimilli

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Isotype and cytotoxicity spectra of anti-lymphocyte antibodies in patients with systemic lupus erythematosus

Cited by 8 publications

References 43 publications

Reversal of lovastatin‐mediated inhibition of natural killer cell cytotoxicity by interleukin 2

Reversal of lovastatin‐mediated inhibition of natural killer cell cytotoxicity by interleukin 2

Endogenous humoral autoreactive immune responses to apoptotic cells: Effects on phagocytic uptake, chemotactic migration and antigenic spread

A synthetic peptide from the third hypervariable region of major histocompatibility complex class II beta chain as a vaccine for treatment of experimental autoimmune encephalomyelitis.

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