Effects of interleukin 12 on immune responses and host protection in mice infected with intestinal nematode parasites.
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- F D Finkelman
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- K B Madden
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- A W Cheever
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- I M Katona
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- S C Morris
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- M K Gately
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- B R Hubbard
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- W C Gause
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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- J F Urban
- Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
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<jats:p>The cytokine interleukin (IL) 12 stimulates T cell and natural killer cell production of interferon (IFN) gamma and inhibits T cell production of IL-4. We investigated the effects of IL-12 on cytokine gene expression, immunoglobulin (Ig)E, mucosal mast cell, and eosinophil responses, and the course of infection in mice inoculated with the nematode parasite Nippostrongylus brasiliensis, as well as the IFN-gamma dependence of these effects. IL-12 stimulated IFN-gamma and IL-10 gene expression during primary and secondary N. brasiliensis infections and inhibited IL-3, IL-4, IL-5, and IL-9 gene expression during primary infections but had little inhibitory effect during secondary infections. IL-12 inhibited IgE, mucosal mast cell, and blood and tissue eosinophil responses during primary infections, but only eosinophil responses during secondary infections. IL-12 enhanced adult worm survival and egg production during primary, but not secondary infections. IL-12 needed to be administered by day 4 of a primary infection to inhibit IgE and mucosal mast cell responses, and by day 6 to strongly inhibit eosinophil responses and to enhance worm survival and fecundity. Anti-IFN-gamma mAb inhibited the effects of IL-12 on IgE secretion, intestinal mucosal mastocytosis, and parasite survival and fecundity, but did not affect IL-12 inhibition of eosinophilia. These observations indicate that IL-12, if administered during the initiation of eosinophilia. These observations indicate that IL-12, if administered during the initiation of an immune response, can change the response from one that is characterized by the production of T helper (Th)2-associated cytokines to one characterized by the production of Th-1 associated cytokines. However, IL-12 treatment has less of an effect once the production of Th2-associated cytokines has become established. In addition, our results provide evidence that Th2-associated responses protect against, and/or Th1-associated responses exacerbate, nematode infections.</jats:p>
収録刊行物
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- The Journal of experimental medicine
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The Journal of experimental medicine 179 (5), 1563-1572, 1994-05-01
Rockefeller University Press
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詳細情報 詳細情報について
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- CRID
- 1363388844197286528
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- NII論文ID
- 30017431839
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- NII書誌ID
- AA00697559
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- ISSN
- 15409538
- 00221007
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