J. Langhorne et al., A ROLE FOR B-CELLS IN THE DEVELOPMENT OF T-CELL HELPER FUNCTION IN A MALARIA INFECTION IN MICE, Proceedings of the National Academy of Sciences of the United Statesof America, 95(4), 1998, pp. 1730-1734
B cell knockout mice are unable to clear a primary erythrocytic infect
ion of Plasmodium chabaudi chabaudi. However, the early acute infectio
n is controlled to some extent, giving rise to a chronic relapsing par
asitemia that can be reduced either by drug treatment or by adoptive t
ransfer of B cells, Similar to mice rendered B-cell deficient by lifel
ong treatment with anti-mu antibodies, B cell knockout mice (mu MT) re
tain a predominant CD4(+) Th1-like response to malarial antigens throu
ghout a primary infection, This contrasts with the response seen in co
ntrol C57BL/6 mice in which the CD4(+) T-cell response has switched to
that characteristic of Th2 cells at the later stages of infection, ma
nifesting efficient help for specific antibodies in vitro and interleu
kin 4 production, Both chloroquine and adoptive transfer of immune B c
ells reduced parasite load, However, the adoptive transfer of B cells
resulted in a Th2 response in recipient mu MT mice, as indicated by a
relative increase in the precursor frequency of helper cells for antib
ody production. These data support the idea that B cells play a role i
n the regulation of CD4(+) T subset responses.