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).