A Role for B Cells in the Development of T Cell Helper Function in a Malaria Infection in Mice

B cell knockout mice are unable to clear a primary erythrocytic infection of Plasmodium chabaudi chabaudi. However, the early acute infection is controlled to some extent, giving rise to a chronic relapsing parasitemia that can be reduced either by drug treatment or by adoptive transfer of B cells....

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Published in:Proceedings of the National Academy of Sciences - PNAS 1998-02, Vol.95 (4), p.1730-1734
Main Authors: Langhorne, Jean, Cross, Caroline, Seixas, Elsa, Li, Ching, Von Der Weid, Thierry
Format: Article
Language:English
Subjects:
Adoptive transfer
Animals
Antibodies
B lymphocytes
B-Lymphocytes - immunology
Biological Sciences
Cells
Chloroquine - therapeutic use
Cytokines
Erythrocytes - parasitology
Female
Genes, Immunoglobulin
Immunoglobulin mu-Chains - genetics
Immunology
Infections
Malaria
Malaria - immunology
Mice
Mice, Knockout
Parasitemia
Parasites
Plasmodium chabaudi - immunology
Pyrimethamine - pharmacology
Rodents
T lymphocytes
T lymphoid precursor cells
T-Lymphocyte Subsets - immunology
Th1 Cells - immunology
Th2 Cells - immunology
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Summary:B cell knockout mice are unable to clear a primary erythrocytic infection of Plasmodium chabaudi chabaudi. However, the early acute infection is controlled to some extent, giving rise to a chronic relapsing parasitemia that can be reduced either by drug treatment or by adoptive transfer of B cells. Similar to mice rendered B-cell deficient by lifelong treatment with anti-μ antibodies, B cell knockout mice (μ MT) retain a predominant CD4+Th1-like response to malarial antigens throughout a primary infection. This contrasts with the response seen in control C57BL/6 mice in which the CD4+T-cell response has switched to that characteristic of Th2 cells at the later stages of infection, manifesting efficient help for specific antibodies in vitro and interleukin 4 production. Both chloroquine and adoptive transfer of immune B cells reduced parasite load. However, the adoptive transfer of B cells resulted in a Th2 response in recipient μ MT mice, as indicated by a relative increase in the precursor frequency of helper cells for antibody production. These data support the idea that B cells play a role in the regulation of CD4+T subset responses.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.95.4.1730