Abstract
Intravenous immunoglobulin (IVIG) has been an important therapy of immune thrombocytopenic purpura (ITP) for more than 20 years; however, questions still remain regarding the mechanisms of IVIG action in ITP. Recent reviews have focused on the hypotheses that IVIG effects are mediated via inhibition of Fc-receptor mediated platelet phagocytosis, suppression of anti-platelet antibody production, and anti-idiotypic inhibition of anti-platelet antibodies; however, new research suggests that a significant portion of IVIG benefit may be due to IVIG-mediated acceleration of the elimination of anti-platelet antibodies. It is anticipated that promising new therapies of ITP, and other autoimmune conditions, will be developed based on a better understanding of IVIG mechanism of action.
| Original language | English |
|---|---|
| Pages (from-to) | 133-140 |
| Number of pages | 8 |
| Journal | Clinical Laboratory |
| Volume | 50 |
| Issue number | 3-4 |
| State | Published - 2004 |
Keywords
- Autoimmune diseases
- Immune thrombocytopenia
- Intravenous immune globulin
- IVIG
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