期刊
SCIENCE ADVANCES
卷 7, 期 41, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abj1249
关键词
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资金
- R03-AI142046-02
- Centers of Excellence for Influenza Virus Research and Surveillance (CEIRS) contract [HHSN272201400008C]
- NIH [U19-AI057234, U19-AI082715, U19-AI089987, R21-AI53673]
- Baylor Health Care System
- Icahn School of Medicine at Mount Sinai
- Advanced Research and Development Programs for Medical Innovation (AMED-CREST) from Japan Agency for Medical Research and Development (AMED)
Tox2 plays a vital role in maintaining T-FH cells and generating memory T-FH cells, while its overexpression can inhibit the spontaneous conversion of T-FH cells into T(H)1-like cells. Tox2 deficiency leads to impaired expansion of secondary T-FH cells upon reimmunization and secondary infection.
Memory T follicular helper (T-FH) cells play an essential role to induce secondary antibody response by providing help to memory and naive B cells. Here, we show that the transcription factor Tox2 is vital for the maintenance of T-FH cells in germinal centers (GCs) and the generation of memory T-FH cells. High Tox2 expression was almost exclusive to GC T-FH cells among human tonsillar and blood CD4(+) T cell subsets. Tox2 overexpression maintained the expression of T-FH-associated genes in T cell receptor-stimulated human GC T-FH cells and inhibited their spontaneous conversion into T(H)1-like cells. Tox2-deficient mice displayed impaired secondary T-FH cell expansion upon reimmunization with an antigen and upon secondary infection with a heterologous influenza virus. Collectively, our study shows that Tox2 is highly integrated into establishment of durable GC T-FH cell responses and development of memory T-FH cells in mice and humans.
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