AI Article Synopsis
- IL-1 is a proinflammatory cytokine vital for the immune response; its absence leads to decreased antibody production against SRBC in IL-1 deficient mice.
- IL-1 deficiency doesn't impair the basic functions of immune cells, but it does hinder the activation of T cells by antigen-presenting cells (APCs).
- Enhanced antibody responses in IL-1 receptor antagonist mice and recovery of antibody production in IL-1 deficient mice after CD40 stimulation suggest that IL-1 boosts T cell activation and antibody production through increased CD40 ligand and OX40 expression.
Article Abstract
IL-1 is a proinflammatory cytokine that plays pleiotropic roles in host defense mechanisms. We investigated the role of IL-1 in the humoral immune response using gene-targeted mice. Ab production against SRBC was significantly reduced in IL-1alpha/beta-deficient (IL-1(-/-)) mice and enhanced in IL-1R antagonist(-/-) mice. The intrinsic functions of T, B, and APCs were normal in IL-1(-/-) mice. However, we showed that IL-1(-/-) APCs did not fully activate DO11.10 T cells, while IL-1R antagonist (-/-) APCs enhanced the reaction, indicating that IL-1 promotes T cell priming through T-APC interaction. The function of IL-1 was CD28-CD80/CD86 independent. We found that CD40 ligand and OX40 expression on T cells was affected by the mutation, and the reduced Ag-specific B cell response in IL-1(-/-) mice was recovered by the treatment with agonistic anti-CD40 mAb both in vitro and in vivo. These observations indicate that IL-1 enhances T cell-dependent Ab production by augmenting CD40 ligand and OX40 expression on T cells.
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| http://dx.doi.org/10.4049/jimmunol.167.1.90 | DOI Listing |
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