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M9650451.TXT
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1996-03-09
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Document 0451
DOCN M9650451
TI Reconstitution of B-cell-depleted mice with B cells restores Th2-type
immune responses during Plasmodium chabaudi chabaudi infection.
DT 9605
AU Taylor-Robinson AW; Phillips RS; Wellcome Laboratories for Experimental
Parasitology, University; of Glasgow, United Kingdom.
SO Infect Immun. 1996 Jan;64(1):366-70. Unique Identifier : AIDSLINE
MED/96110959
AB In mice depleted of B cells from birth by treatment with
anti-immunoglobulin M(mu) antibodies, progression from a Th1- to a
Th2-regulated immune response during primary infection with Plasmodium
chabaudi chabaudi fails to occur. While Th1-type immunity limits
parasitemia, in the absence of B cells, chronic low-grade infections
persist. Here, we show that reconstituting immune, and to a lesser
extent naive, B cells to mice rendered deficient in B-cell function
through anti-immunoglobulin M(mu) pretreatment restores the CD4+ T-cell
response to the Th2 type later in P. c. chabaudi infection and with it
the capacity to eliminate infection. This finding provides clear
evidence that B cells are required for switching the balance of immune
regulation between CD4+ T cells from Th1 to Th2 during P.c. chabaudi
infection and supports the concept that B cells, through antibody
production, are needed for effective antimalarial immunity.
DE Animal Antibodies, Protozoan/BLOOD B-Lymphocytes/*IMMUNOLOGY
CD4-Positive T-Lymphocytes/METABOLISM Female Immunity Immunoglobulin
Isotypes/BLOOD Immunoglobulins, mu-Chain/IMMUNOLOGY Immunotherapy,
Adoptive Interferon Type II/BIOSYNTHESIS Interleukins/BIOSYNTHESIS
Lymphocyte Depletion Malaria/*VETERINARY Mice Plasmodium
chabaudi/*IMMUNOLOGY Rodent Diseases/*IMMUNOLOGY
Spleen/CYTOLOGY/IMMUNOLOGY Support, Non-U.S. Gov't Th1
Cells/IMMUNOLOGY Th2 Cells/*IMMUNOLOGY Treatment Outcome JOURNAL
ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).