Your browser version may not work well with NCBI's Web applications. More information here...
1: J Immunol. 2007 Sep 15;179(6):4093-100.
Related Articles, Links
Click here to read Click here to read
Ligation of B and T lymphocyte attenuator prevents the genesis of experimental cerebral malaria.

Lepenies B, Pfeffer K, Hurchla MA, Murphy TL, Murphy KM, Oetzel J, Fleischer B, Jacobs T.

Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.

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.

Publication Types:
PMID: 17785848 [PubMed - indexed for MEDLINE]