Abstract
We evaluated the mechanism by which human pooled γ-globulin for intravenous use (hIVIG) inhibits interleukin-2 (IL-2) production by human T cells. hIVIG reduced by 70-95% the amount of IL-2 in culture supernatants from mitogen-stimulated peripheral blood T cells or Jurkat cells. This reduction was not apparent at the transcriptional level: hIVIG had no effect on the levels of IL-2 mRNA or on the accumulation of firefly luciferase when its gene was linked to the IL-2 promoters. In contrast, hIVIG inhibited IL-2 protein synthesis, and the intracellular IL-2 was not restored by monensin. Our results indicate that the inhibition of IL-2 production by hIVIG occurred posttranscriptionally, and also suggest that secretion was unaffected, and that this effect of hIVIG was specific for IL-2 (and possibly other related cytokines). The data identify a previously uncharacterized regulatory mechanism of IL-2 production and predict that this immunomodulatory effect of hIVIG may be significant for its therapeutic actions in immune-mediated diseases.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 77-85 |
| Number of pages | 9 |
| Journal | Clinical Immunology and Immunopathology |
| Volume | 83 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 1 1997 |
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Posttranscriptional regulation of T-cell IL-2 production by human pooled immunoglobin. / Modiano, Jaime F.; Amran, David; Lack, Gideon; Bradley, Katherine; Ball, Carrie; Domenico, Joanne; Gelfand, Erwin W.
In: Clinical Immunology and Immunopathology, Vol. 83, No. 1, 01.01.1997, p. 77-85.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Posttranscriptional regulation of T-cell IL-2 production by human pooled immunoglobin
AU - Modiano, Jaime F.
AU - Amran, David
AU - Lack, Gideon
AU - Bradley, Katherine
AU - Ball, Carrie
AU - Domenico, Joanne
AU - Gelfand, Erwin W.
PY - 1997/1/1
Y1 - 1997/1/1
N2 - We evaluated the mechanism by which human pooled γ-globulin for intravenous use (hIVIG) inhibits interleukin-2 (IL-2) production by human T cells. hIVIG reduced by 70-95% the amount of IL-2 in culture supernatants from mitogen-stimulated peripheral blood T cells or Jurkat cells. This reduction was not apparent at the transcriptional level: hIVIG had no effect on the levels of IL-2 mRNA or on the accumulation of firefly luciferase when its gene was linked to the IL-2 promoters. In contrast, hIVIG inhibited IL-2 protein synthesis, and the intracellular IL-2 was not restored by monensin. Our results indicate that the inhibition of IL-2 production by hIVIG occurred posttranscriptionally, and also suggest that secretion was unaffected, and that this effect of hIVIG was specific for IL-2 (and possibly other related cytokines). The data identify a previously uncharacterized regulatory mechanism of IL-2 production and predict that this immunomodulatory effect of hIVIG may be significant for its therapeutic actions in immune-mediated diseases.
AB - We evaluated the mechanism by which human pooled γ-globulin for intravenous use (hIVIG) inhibits interleukin-2 (IL-2) production by human T cells. hIVIG reduced by 70-95% the amount of IL-2 in culture supernatants from mitogen-stimulated peripheral blood T cells or Jurkat cells. This reduction was not apparent at the transcriptional level: hIVIG had no effect on the levels of IL-2 mRNA or on the accumulation of firefly luciferase when its gene was linked to the IL-2 promoters. In contrast, hIVIG inhibited IL-2 protein synthesis, and the intracellular IL-2 was not restored by monensin. Our results indicate that the inhibition of IL-2 production by hIVIG occurred posttranscriptionally, and also suggest that secretion was unaffected, and that this effect of hIVIG was specific for IL-2 (and possibly other related cytokines). The data identify a previously uncharacterized regulatory mechanism of IL-2 production and predict that this immunomodulatory effect of hIVIG may be significant for its therapeutic actions in immune-mediated diseases.
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U2 - 10.1006/clin.1997.4329
DO - 10.1006/clin.1997.4329
M3 - Article
VL - 83
SP - 77
EP - 85
JO - Clinical Immunology
JF - Clinical Immunology
SN - 1521-6616
IS - 1
ER -