Paxbp1 is indispensable for the maintenance of peripheral CD4 T cell homeostasis

Author:

Li Wenting12ORCID,Yang Yang3,Zhuo Fan12,Liu Shenglin4,Zhang Kaoyuan12,Zhang Wei35,Huang Cong12,Yu Bo12

Affiliation:

1. Department of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong Province China

2. Shenzhen Key Laboratory for Translational Medicine of Dermatology Shenzhen Peking University ‐ The Hong Kong University of Science and Technology Medical Center Shenzhen Guangdong Province China

3. Biomedical Research Institute Shenzhen Peking University ‐ The Hong Kong University of Science and Technology Medical Center Shenzhen China

4. Key Laboratory of Research and Utilization of Ethnomedicinal Plant Resources of Hunan Province, College of Biological and Food Engineering Huaihua University Huaihua Hunan Province China

5. Greater Bay Biomedical Innocenter Shenzhen Bay Laboratory Shenzhen Guangdong Province China

Abstract

AbstractThe size and condition of the peripheral CD4 T cell population determine the capacity of the immune response. Under homeostatic conditions, the size of the peripheral CD4 T cell population is maintained through turnover and survival. However, the underlying mechanisms remain inadequately understood. Here, we observed a significant decrease in the percentage of CD4 T cells in the periphery following the targeted deletion of the Paxbp1 gene in mouse T cells. In the absence of Paxbp1, naïve CD4 T cells displayed reduced surface interleukin‐7 receptor levels and a decreased capacity to respond to survival signals mediated by interleukin‐7. In addition, naïve CD4 T cells deficient in Paxbp1 demonstrated impaired T cell antigen receptor signalling, compromised cell cycle entry, decreased proliferation, and increased apoptosis following stimulation, all of which contributed to the reduction in the number of peripheral CD4 T cells. Therefore, our study highlights the indispensable role of Paxbp1 in maintaining peripheral CD4 T cell homeostasis.

Funder

Basic and Applied Basic Research Foundation of Guangdong Province

National Natural Science Foundation of China

Publisher

Wiley

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