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The adaptor protein SAP regulates type II NKT-cell development, cytokine production, and cytotoxicity against lymphoma.

Artikel i vetenskaplig tidskrift
Författare Xiufang Weng
Chia-Min Liao
Susanna Cardell
Sreya Bagchi
Paul L Stein
Chyung-Ru Wang
Publicerad i European journal of immunology
Volym 44
Nummer/häfte 12
Sidor 3646–3657
ISSN 1521-4141
Publiceringsår 2014
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 3646–3657
Språk en
Länkar dx.doi.org/10.1002/eji.201444848
Ämnesord CD1d, NKT, lymphoma
Ämneskategorier Immunbiologi

Sammanfattning

CD1d-restricted NKT cells represent a unique lineage of immunoregulatory T cells that are divided into two groups, type I and type II, based on their TCR usage. Because there are no specific tools to identify type II NKT cells, little is known about their developmental requirements and functional regulation. In our previous study, we showed that signaling lymphocytic activation molecule associated protein (SAP) is essential for the development of type II NKT cells. Here, using a type II NKT-cell TCR transgenic mouse model, we demonstrated that CD1d-expressing hematopoietic cells, but not thymic epithelial cells, meditate efficient selection of type II NKT cells. Furthermore, we showed that SAP regulates type II NKT-cell development by controlling early growth response 2 protein and promyelocytic leukemia zinc finger expression. SAP-deficient 24αβ transgenic T cells (24αβ T cells) exhibited an immature phenotype with reduced Th2 cytokine-producing capacity and diminished cytotoxicity to CD1d-expressing lymphoma cells. The impaired IL-4 production by SAP-deficient 24αβ T cells was associated with reduced IFN regulatory factor 4 and GATA-3 induction following TCR stimulation. Collectively, these data suggest that SAP is critical for regulating type II NKT cell responses. Aberrant responses of these T cells may contribute to the immune dysregulation observed in X-linked lymphoproliferative disease caused by mutations in SAP.

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