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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1996-9-16
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pubmed:abstractText |
We studied the potential role of B cells in T cell responses using severe-combined immunodeficient (SCID) mice grafted with the thymus from fetal C.B-17 mice (TG mice). These mice developed both CD4+ and CD8+ T cells, but not B cells within 2 months after transplantation. TG mice showed normal delayed-type hypersensitivity responses against the immunizing antigen ovalbumin (OVA). Lymph node (LN) cells of TG mice proliferated well in response to concanavalin A (Con A). Further, Con A stimulation induced the production of interleukin (IL)-2, IL-6 and interferon (IFN)-gamma and the expression of IL-4 mRNA. Thus, TG mice were reconstituted without remarkable immunodeficiency. However, these T cells failed to proliferate to OVA stimulation. Response to OVA was also inhibited in SCID mice grafted with fetal C.B-17 liver cells when B cells were depleted in the proliferation assay. Unresponsiveness against immunizing antigen was restored by the addition of antigen-primed B cells, but not by naive B cells, lipopolysaccharide-activated B cells or B cells primed with sheep red blood cells. Next, we examined whether antigen-primed B cells could induce T cell responses without professional antigen-presenting cells (APC). T and B cells were purified from OVA-immunized mice by cell sorter. These T cells proliferated in response to OVA and produced IFN-gamma in the absence of non-B APC. When anti-CD80 or anti-CD86 was added in the assay, proliferation and IFN-gamma production was inhibited. These results indicate that B cells activated specifically with antigen are required for the secondary response of T cells, but not for their priming.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1628-33
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:8766571-Animals,
pubmed-meshheading:8766571-Antigen-Presenting Cells,
pubmed-meshheading:8766571-Antigens, CD28,
pubmed-meshheading:8766571-Antigens, CD80,
pubmed-meshheading:8766571-B-Lymphocytes,
pubmed-meshheading:8766571-Epitopes,
pubmed-meshheading:8766571-Fetal Tissue Transplantation,
pubmed-meshheading:8766571-Hematopoiesis,
pubmed-meshheading:8766571-Hypersensitivity, Delayed,
pubmed-meshheading:8766571-Immunization, Secondary,
pubmed-meshheading:8766571-Liver Transplantation,
pubmed-meshheading:8766571-Lymphocyte Activation,
pubmed-meshheading:8766571-Mice,
pubmed-meshheading:8766571-Mice, SCID,
pubmed-meshheading:8766571-Ovalbumin,
pubmed-meshheading:8766571-T-Lymphocytes,
pubmed-meshheading:8766571-Thymus Gland
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pubmed:year |
1996
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pubmed:articleTitle |
Antigen-specific B cells are required for the secondary response of T cells but not for their priming.
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pubmed:affiliation |
Department of Parasitology and Immunology, School of Medicine, University of Tokushima, Japan.
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pubmed:publicationType |
Journal Article
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