| First Author | Lepenies B | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 6 | Pages | 4093-100 |
| PubMed ID | 17785848 | Mgi Jnum | J:152027 |
| Mgi Id | MGI:4355789 | Doi | 10.4049/jimmunol.179.6.4093 |
| Citation | Lepenies B, et al. (2007) Ligation of B and T lymphocyte attenuator prevents the genesis of experimental cerebral malaria. J Immunol 179(6):4093-100 |
| abstractText | B and T lymphocyte attenuator (BTLA; CD272) is a coinhibitory receptor that is predominantly expressed on T and B cells and dampens T cell activation. In this study, we analyzed the function of BTLA during infection with Plasmodium berghei ANKA. Infection of C57BL/6 mice with this strain leads to sequestration of leukocytes in brain capillaries that is associated with a pathology resembling cerebral malaria in humans. During the course of infection, we found an induction of BTLA in several organs, which was either due to up-regulation of BTLA expression on T cells in the spleen or due to infiltration of BTLA-expressing T cells into the brain. In the brain, we observed a marked induction of BTLA and its ligand herpesvirus entry mediator during cerebral malaria, which was accompanied by an accumulation of predominantly CD8+ T cells, but also CD4+ T cells. Application of an agonistic anti-BTLA mAb caused a significantly reduced incidence of cerebral malaria compared with control mice. Treatment with this Ab also led to a decreased number of T cells that were sequestered in the brain of P. berghei ANKA-infected mice. Our findings indicate that BTLA-herpesvirus entry mediator interactions are functionally involved in T cell regulation during P. berghei ANKA infection of mice and that BTLA is a potential target for therapeutic interventions in severe malaria. |
