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Dendritic cell expression of CD24 contributes to optimal priming of T lymphocytes in lymph nodes
Xuejun Zhang1, Chuan Yu1, Jin-Qing Liu1
1Department of Pathology and Comprehensive Cancer Center, The Ohio State University Medical Center, Columbus, OH, United States.
Insights
CD24 on dendritic cells is crucial for effective T cell priming. Its absence impairs T cell expansion and survival, suggesting CD24 blockade could treat autoimmune diseases.
Area of Science:
- Immunology
- Cell Biology
Background:
- CD24 is a cell surface glycoprotein with known co-stimulatory roles.
- The specific function of CD24 on antigen-presenting cells in T cell responses remains unclear.
Purpose of the Study:
- To investigate the role of CD24 on dendritic cells in T cell priming.
- To determine the impact of CD24 deficiency on T cell expansion and survival.
Main Methods:
- Utilized CD24-deficient mice and adoptive T cell transfer.
- Assessed T cell accumulation, survival, and antigen-specific responses using MHC II tetramer staining.
- Investigated potential anti-CD24 immune responses.
Main Results:
- CD24-deficient hosts showed inefficient CD4+ T cell expansion and increased cell death in lymph nodes.
- T cell priming was insufficient in CD24-deficient mice.
- Restoring CD24 on dendritic cells in CD24-/- mice normalized T cell accumulation and survival.
- Antigen-specific T cell responses were reduced in CD24-/- mice.
Conclusions:
- CD24 on dendritic cells plays a critical role in optimal T cell priming within lymph nodes.
- CD24 blockade may be a therapeutic strategy to mitigate unwanted T cell responses in autoimmune conditions.
Abstract:
CD24 is a GPI anchored cell surface glycoprotein whose function as a co-stimulatory molecule has been implicated. However, the function of CD24 on antigen presenting cells during T cell responses is not well understood. Here we show that in the CD24-deficient host, adoptively transferred CD4+ T cells undergo inefficient expansion and have accelerated cell death in lymph nodes, which results in insufficient priming of T cells. Insufficient expansion of T cells in the CD24-deficient host was not due to host anti-CD24 response by NK, T and B lymphocytes. Transgenic expression of CD24 on DC in CD24-/- mice restored T cell accumulation and survival in draining lymph nodes. Consistent with these findings, MHC II tetramer staining also revealed that an antigen-specific polyclonal T cell response was reduced in lymph nodes of CD24-/- mice. Taken together, we have revealed a novel role of CD24 on DC in optimal T cell priming in lymph nodes. These data suggest that CD24 blockade should lower unwanted T cell responses such as those in autoimmune diseases.
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