The Journal of Experimental Medicine
Randox
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Published online 31 March 2003 doi:10.1084/jem.20021290
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© Rockefeller University Press, 0022-1007/2003/4/875 $5.00
The Journal of Experimental Medicine, Volume 197, Number 7, 875-883

Costimulation via OX40L Expressed by B Cells Is Sufficient to Determine the Extent of Primary CD4 Cell Expansion and Th2 Cytokine Secretion In Vivo

Phyllis-Jean Linton, Beverly Bautista, Elana Biederman, Evan S. Bradley, Judith Harbertson, Robyn M. Kondrack, Ryan C. Padrick and Linda M. Bradley

The Sidney Kimmel Cancer Center, San Diego, CA 92121

Address correspondence to Linda M. Bradley, The Sidney Kimmel Cancer Center, 10835 Altman Row, San Diego, CA 92121. Phone: 858-410-4213; Fax: 858-450-3251; E-mail: lbradley{at}skcc.org

The development of effector and memory CD4 cell populations depends upon both T cell receptor (TCR) engagement of peptide/major histocompatibility complex (MHC) class II complexes and ligation of costimulatory molecules with counter receptors on antigen-presenting cells (APCs). We showed previously that sustained interactions with APCs could be crucial for optimal expansion of CD4 cells and for development of effectors that secrete cytokines associated with Th2 cells. Using an adoptive transfer model with TCR transgenic CD4 cells, we now show that responses of CD4 cells primed in B cell–deficient mice become aborted, but are fully restored upon the transfer of activated B cells. Although B cells have the capacity to secrete multiple cytokines that could affect CD4 priming, including IL-4, we were unable to distinguish a role for cytokines that are secreted by B cells. However, B cell costimulation via the OX40L/OX40 pathway that has been implicated in CD4 cell expansion, survival, and Th2 development was required. Th2 but not Th1 responses were impaired in OX40L-deficient recipients and normal responses were restored with OX40L sufficient B cells. The results suggest that without engagement of OX40L on B cells, CD4 cell responses to many protein Ag would be dominated by Th1 cytokines. These data have important implications for strategies to achieve optimal priming of CD4 subsets.

Key Words: CD4 subsets • B lymphocytes • antigen-presenting cells • cytokines • Th2 cells


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