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*
Third Department of Internal Medicine,
Department of Immunology and Medical Zoology, and
Laboratory of Host Defenses Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan;
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Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan;
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Department of Parasitology, Institute of Medical Science, University of Tokyo, Tokyo, Japan; and
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Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo, Japan
Infection with Schistosoma mansoni, a portal
vein-residing helminth, is well known to generate life cycle-dependent,
systemic immune responses in the host, type 1 deviation during the
prepatent period, and type 2 polarization after oviposition. Here we
investigated local immunological changes in the liver after infection.
Unlike splenocytes, hepatic lymphocytes from infected mice during the
prepatent period already produced a higher amount of IL-4 and a lesser
amount of IFN-
than those from uninfected mice. Hepatic lymphocytes,
particularly conventional T cells, but not NK1.1+ T cells,
promptly produced IL-4 in response to worm products, soluble worm Ag
preparation (SWAP), whenever presented by Kupffer cells from infected
mice. The hepatic lymphocytes that had been stimulated with SWAP
presented by infected mice-derived Kupffer cells produced a huge amount
of IL-4, IL-13, and IL-5 as well as little IFN- in response to
immobilized anti-CD3 mAb. Kupffer cells from uninfected mice
produced IL-6 and IL-10, but not IL-12 or IL-18, in response to SWAP
stimulation and gained the potential to additionally produce IL-4 and
IL-13 after the infection. These results suggested that prompt type 2
deviation in the liver after the infection might be due to the
alteration of Kupffer cells that induces SWAP-mediated type
2-development of hepatic T cells.
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