A role for IL-1 receptor antagonist or other cytokines in the acute therapeutic effects of IVIg?
(2007) In Blood 109(1). p.155-158- Abstract
The exact mechanism of action of IVIg in the amelioration of immune thrombocytopenic purpura (ITP) is still unclear. Studies have suggested that IVIg may function through the regulation of cytokines, including interleukin-1 receptor antagonist (IL-1Ra), an inhibitor of phagocytosis. Using a mouse model relevant to ITP, we confirm an increase in mouse serum levels of IL-1Ra after exposure to IVIg, yet a recombinant IL-1Ra did not ameliorate thrombocytopenia. IVIg has also been shown to affect the expression of other regulatory cytokines. We have also recently established that IVIg specifically targets activating FcγRs on CD11c+ dendritic cells (DCs) as its primary mechanism of action in the amelioration of murine ITP. Herein,... (More)
The exact mechanism of action of IVIg in the amelioration of immune thrombocytopenic purpura (ITP) is still unclear. Studies have suggested that IVIg may function through the regulation of cytokines, including interleukin-1 receptor antagonist (IL-1Ra), an inhibitor of phagocytosis. Using a mouse model relevant to ITP, we confirm an increase in mouse serum levels of IL-1Ra after exposure to IVIg, yet a recombinant IL-1Ra did not ameliorate thrombocytopenia. IVIg has also been shown to affect the expression of other regulatory cytokines. We have also recently established that IVIg specifically targets activating FcγRs on CD11c+ dendritic cells (DCs) as its primary mechanism of action in the amelioration of murine ITP. Herein, we show that IVIg functions therapeutically in mice lacking specific cytokines or their receptors that can potentially affect DC/macrophage function (IL-1 receptor, IL-4, IL-10, IL-12β, TNF-α, IFN-γ receptor, MIP-1α). This suggests that while IVIg may mediate the release of a variety of cytokines, the cytokines tested do not directly participate in the mechanism of IVIg action.
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- author
- Crow, Andrew R. ; Song, Seng ; Semple, John W. LU ; Freedman, John and Lazarus, Alan H.
- publishing date
- 2007-01-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 109
- issue
- 1
- pages
- 155 - 158
- publisher
- American Society of Hematology
- external identifiers
-
- pmid:16954498
- scopus:33845976292
- ISSN
- 0006-4971
- DOI
- 10.1182/blood-2006-05-023796
- language
- English
- LU publication?
- no
- id
- 2a23df4f-8c81-4a01-a883-855c91c96042
- date added to LUP
- 2019-12-03 10:19:33
- date last changed
- 2024-10-02 17:33:15
@article{2a23df4f-8c81-4a01-a883-855c91c96042, abstract = {{<p>The exact mechanism of action of IVIg in the amelioration of immune thrombocytopenic purpura (ITP) is still unclear. Studies have suggested that IVIg may function through the regulation of cytokines, including interleukin-1 receptor antagonist (IL-1Ra), an inhibitor of phagocytosis. Using a mouse model relevant to ITP, we confirm an increase in mouse serum levels of IL-1Ra after exposure to IVIg, yet a recombinant IL-1Ra did not ameliorate thrombocytopenia. IVIg has also been shown to affect the expression of other regulatory cytokines. We have also recently established that IVIg specifically targets activating FcγRs on CD11c<sup>+</sup> dendritic cells (DCs) as its primary mechanism of action in the amelioration of murine ITP. Herein, we show that IVIg functions therapeutically in mice lacking specific cytokines or their receptors that can potentially affect DC/macrophage function (IL-1 receptor, IL-4, IL-10, IL-12β, TNF-α, IFN-γ receptor, MIP-1α). This suggests that while IVIg may mediate the release of a variety of cytokines, the cytokines tested do not directly participate in the mechanism of IVIg action.</p>}}, author = {{Crow, Andrew R. and Song, Seng and Semple, John W. and Freedman, John and Lazarus, Alan H.}}, issn = {{0006-4971}}, language = {{eng}}, month = {{01}}, number = {{1}}, pages = {{155--158}}, publisher = {{American Society of Hematology}}, series = {{Blood}}, title = {{A role for IL-1 receptor antagonist or other cytokines in the acute therapeutic effects of IVIg?}}, url = {{http://dx.doi.org/10.1182/blood-2006-05-023796}}, doi = {{10.1182/blood-2006-05-023796}}, volume = {{109}}, year = {{2007}}, }