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Open Access Research article

BATF regulates the development and function of IL-17 producing iNKT cells

Kimberly L Jordan-Williams1, Stacie Poston1 and Elizabeth J Taparowsky2*

Author Affiliations

1 Department of Biological Sciences and Purdue University Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA

2 Department of Biological Sciences, Hansen Life Sciences Research Building, Room 219, 201 South University Street, West Lafayette, IN, USA

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BMC Immunology 2013, 14:16  doi:10.1186/1471-2172-14-16

Published: 27 March 2013

Abstract

Background

BATF plays important roles in the function of the immune system. Batf null mice are deficient in both CD4+ Th17 cells and T follicular helper cells and possess an intrinsic B cell defect that leads to the complete absence of class switched Ig. In this study, Tg mice overexpressing BATF in T cells were used together with Batf null mice to investigate how altering levels of BATF expression in T cells impacts the development and function of a recently characterized population of iNKT cells expressing IL-17 (iNKT-17).

Results

BATF has a direct impact on IL-17 expression by iNKT cells. However, in contrast to the Th17 lineage where BATF activates IL-17 expression and leads to the expansion of the lineage, BATF overexpression restricts overall iNKT cell numbers while skewing the compartment in vivo and in vitro toward an iNKT-17 phenotype.

Conclusions

This work is the first to demonstrate that BATF joins RORĪ³t as the molecular signature for all IL-17 producing cells in vivo and identifies BATF as a component of the nuclear protein network that could be targeted to regulate IL-17-mediated disease. Interestingly, these studies also reveal that while the Il17a gene is a common target for BATF regulation in Th17 and iNKT-17 cells, this regulation is accompanied by opposite effects on the growth and expansion of these two cell lineages.

Keywords:
BATF; Activator-protein-1; iNKT cells; IL-17; Mouse models