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Prepublished online as a Blood First Edition Paper on April 24, 2003; DOI 10.1182/blood-2002-08-2416. This Article Full Text (PDF) All Versions of this Article: 2002-08-2416v1 102/4/1381    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wong, S.-C. Articles by Lam, K.-P. Search for Related Content PubMed PubMed Citation Articles by Wong, S.-C. Articles by Lam, K.-P. Social Bookmarking                   What's this? Submitted August 9, 2002 Accepted April 5, 2003 Impaired germinal center formation and recall T-cell-dependent immune responses in mice lacking the co-stimulatory ligand B7-H2 Siew-Cheng Wong, Edwin Oh, Chee-Hoe Ng, and Kong-Peng Lam* Department of Molecular and Cellular Immunology, Institute of Molecular and Cell Biology, Singapore, Singapore * Corresponding author; email: mcblamkp{at}imcb.nus.edu.sg. B7-H2, which is expressed constitutively on B cells and binds the inducible co-stimulator (ICOS) on antigen-activated T cells, is a member of the B7 family of co-stimulatory ligands. We have inactivated B7-H2 in the mouse. B7-H2-/- mice generate normal populations of B and T cells in their various lymphoid organs but have lower basal levels of heavy chain class-switched antibodies in their sera. These mice are able to mount normal immune responses to both type I and type II T cell-independent antigens. However, their pattern of responses to a T cell-dependent antigen is altered with greatly reduced production of antigen-specific heavy chain class-switched antibodies, the levels of which could not be elevated even with repeated immunizations. This suggests a critical role for B7-H2 in the recall phases of the immune response. Germinal center formation is also impaired in the mutant mice. While B cells from the mutant mice could response normally to anti-IgM, anti-CD40 as well as LPS stimulation, the production of T-helper-type II cytokines such as IL-4 and IL-10 by primed CD4+ T cells from mutant mice were reduced. This indicated that the defects in humoral responses and germinal centers formation in B7-H2-deficient mice are due to the lack of T cell-mediated help to the B cells. Hence, B7-H2 on B cells is important for recruiting T cell help via its interaction with ICOS and plays a critical role in co-stimulating humoral immune responses. 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