CD5NK1.1+ γδ T Cells that Develop in a Bcl11b-Independent Manner Participate in Early Protection against Infection

Shinya Hatano, Tesshin Murakami, Naoto Noguchi, Hisakata Yamada, Yasunobu Yoshikai

Research output: Contribution to journalArticle

Abstract

We recently found that a unique subset of innate-like γδ T cells develops from the DN2a stage of the fetal thymus independently of the zinc-finger transcription factor B cell leukemia/lymphoma 11b (Bcl11b). Herein, we characterize these Bcl11b-independent γδ T cells in the periphery as CD5NK1.1+ and Granzyme B+, and we show that they are capable of producing interferon (IFN)-γ upon T cell receptor stimulation without Ca2+ influx. In wild-type mice, these cells were sparse in lymphoid tissues but abundant in non-lymphoid tissues, such as the liver. Bcl11b-independent CD5NK1.1+ γδ T cells appeared and contributed to early protection before Bcl11b-dependent CD5+NK1.1 γδ T cells following Listeria monocytogenes infection, resembling their sequential appearance during development in the thymus. Bcl11b is essential for transition from the DN2a to the DN2b stage in the thymus. Hatano et al. find that CD5NK1.1+ γδ T cells develop from the DN2a stage in a Bcl11b-independent manner and participate in host defense at an early stage after bacterial infection in periphery.

Original languageEnglish
Pages (from-to)1191-1202
Number of pages12
JournalCell Reports
Volume21
Issue number5
DOIs
Publication statusPublished - Oct 31 2017

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B-Cell Leukemia
T-cells
B-Cell Lymphoma
Thymus
T-Lymphocytes
Infection
Thymus Gland
Tissue
Listeria
Granzymes
Complement Factor B
Listeriosis
T-Cell Antigen Receptor
Liver
Zinc Fingers
Interferons
Listeria monocytogenes
Lymphoid Tissue
Zinc
Bacterial Infections

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

CD5NK1.1+ γδ T Cells that Develop in a Bcl11b-Independent Manner Participate in Early Protection against Infection. / Hatano, Shinya; Murakami, Tesshin; Noguchi, Naoto; Yamada, Hisakata; Yoshikai, Yasunobu.

In: Cell Reports, Vol. 21, No. 5, 31.10.2017, p. 1191-1202.

Research output: Contribution to journalArticle

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