Compromised OX40 function in CD28-deficient mice is linked with failure to develop CXC chemokine receptor 5-positive CD4 cells and germinal centers.
J Exp Med
; 190(8): 1115-22, 1999 Oct 18.
Article
em En
| MEDLINE
| ID: mdl-10523609
ABSTRACT
Mice rendered deficient in CD28 signaling by the soluble competitor, cytotoxic T lymphocyte-associated molecule 4-immunoglobulin G1 fusion protein (CTLA4-Ig), fail to upregulate OX40 expression in vivo or form germinal centers after immunization. This is associated with impaired interleukin 4 production and a lack of CXC chemokine receptor (CXCR)5 on CD4 T cells, a chemokine receptor linked with migration into B follicles. Germinal center formation is restored in CTLA4-Ig transgenic mice by coinjection of an agonistic monoclonal antibody to CD28, but this is substantially inhibited if OX40 interactions are interrupted by simultaneous injection of an OX40-Ig fusion protein. These data suggest that CD28-dependent OX40 ligation of CD4 T cells at the time of priming is linked with upregulation of CXCR5 expression, and migration of T cells into B cell areas to support germinal center formation.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Receptores do Fator de Necrose Tumoral
/
Receptores de Citocinas
/
Antígenos CD28
/
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral
/
Imunoconjugados
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
Reino Unido