| First Author | Langhorne J | Year | 1998 |
| Journal | Proc Natl Acad Sci U S A | Volume | 95 |
| Issue | 4 | Pages | 1730-4 |
| PubMed ID | 9465085 | Mgi Jnum | J:120241 |
| Mgi Id | MGI:3704079 | Doi | 10.1073/pnas.95.4.1730 |
| Citation | Langhorne J, et al. (1998) A role for B cells in the development of T cell helper function in a malaria infection in mice. Proc Natl Acad Sci U S A 95(4):1730-4 |
| abstractText | 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-mu antibodies, B cell knockout mice (muMT) 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 muMT 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. |
