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M9650426.TXT
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1996-03-09
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Document 0426
DOCN M9650426
TI IL-12, as an adjuvant, promotes a T helper 1 cell, but does not suppress
a T helper 2 cell recall response.
DT 9605
AU Bliss J; Van Cleave V; Murray K; Wiencis A; Ketchum M; Maylor R; Haire
T; Resmini C; Abbas AK; Wolf SF; Genetics Institute Inc., Cambridge, MA
02140, USA.
SO J Immunol. 1996 Feb 1;156(3):887-94. Unique Identifier : AIDSLINE
MED/96144306
AB IL-12 is a potent inducer of NK and cytolytic T cell activity, IFN-gamma
production, and T cell proliferation, and is necessary for
differentiation of naive T cells to the Th1 subset. We have previously
shown that IL-12 promotes a primary Th1 response and suppresses a
primary Th2 response in lymph nodes of mice primed with a model
hapten-protein conjugate, 2,4,6-trinitrophenyl (TNP)-keyhole limpet
hemocyanin (KLH). We have now extended these studies to determine the Th
phenotype of the recall response following immunization with soluble Ag
and IL-12. For these experiments, mice were primed with TNP-KLH with or
without treatment with IL-12, allowed to progress beyond the primary
immune response, and challenged by i.p. injection of TNP-KLH. The
phenotype of the recall response was monitored by measuring ex vivo
production of IFN-gamma and IL-4 in Ag-stimulated lymph node and spleen
cell cultures. Titer and isotype of TNP-specific serum Abs were also
evaluated. Mice primed with Ag+IL-12 developed a Th1 recall response, as
detected by KLH-specific IFN-gamma production from cultured spleen cells
and the presence of TNP-specific IgG2a Ab in serum. However, they also
developed an Ag-specific Th2 recall response, as characterized by
Ag-induced IL-4 production from spleen cells and the presence of high
titers of anti-TNP IgG1 in the serum. Studies of the cytokine profile
during the primary response revealed that IL-12 induced in spleen cells
the capacity to express both IL-4 and IFN-gamma. CD4+ T cells are
necessary for production of IL-4 in the spleens of IL-12-treated mice,
and most likely account for the Th2 recall response detected in mice
primed with Ag+IL-12. These results indicate that the Th1 phenotype
induced by immunization with IL-12 and Ag is maintained so that a Th1
recall response is expressed upon subsequent challenge with Ag. However,
immunization with IL-12 also supports the development of a Th2 recall
response, indicating that the Th1-inducing effect of IL-12 in vivo is
not accompanied by a long lasting suppression of Th2 development.
DE Adjuvants, Immunologic/*PHARMACOLOGY Animal Antibody Specificity
Female Hemocyanin/IMMUNOLOGY IgG/BIOSYNTHESIS Immunologic
Memory/*DRUG EFFECTS Interleukin-12/*PHARMACOLOGY
Interleukin-4/BIOSYNTHESIS Lymph Nodes/IMMUNOLOGY Mice Mice, Inbred
BALB C Mice, Inbred C57BL Mollusca Spleen/IMMUNOLOGY Th1 Cells/*DRUG
EFFECTS/IMMUNOLOGY/METABOLISM Th2 Cells/*DRUG
EFFECTS/IMMUNOLOGY/METABOLISM Trinitrobenzenes/IMMUNOLOGY JOURNAL
ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).