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Transduction of Batf family members provide distinct functions to mouse CD8+ T cells.

ABSTRACT: BATF family members including BATF, BATF2, and BATF3 has critical roles in various types of immune cells. Several studies have indicated that their functions are redundant as they can compensate for each other’s functions. Here, we show that transduction of Batf family members confers distinct characteristics on CD8+ T cells. Batf- and Batf2-transduced CD8+ T cells exhibited effector and memory-like phenotypes, respectively. Intriguingly, Batf3-transduced CD8+ T cells showed effector- and memory-like phenotypes in response to effector- and memory-associated cytokines, respectively and superior anti-tumor activity in vivo among BATF family members. Our results demonstrated that each BATF family member has distinct functions in CD8+ T cells. These findings help us understand the roles of BATF family members in CD8+ T cells and contribute to the development of optimized adoptive T cell therapies against cancer.

ORGANISM(S): Mus musculus

PROVIDER: GSE273727 | GEO | 2026/04/02

REPOSITORIES: GEO

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Project description:Inducing the long-term protection via effector memory CD8+ T cells residing in the peripheral tissues is the ultimate goal of T cell-based vaccination strategies. CD8+ T cell reacting against a particular set of antigenic peptides show propensity to generate stable pools of memory inflating cells with profound protective capacity. While the epitopes that induce memory inflation have been thoroughly characterized and used as excellent constituents of vaccines such as recombinant adenoviruses, the identity of the tissue factors responsible for maintaining memory inflating CD8+ T cells remains elusive. Here, we have used a Cre recombinase-dependent, -galactosidase (gal)–recombinant adenovirus vector that allowed for cell-specific expression of gal epitopes and identification of cell types involved in generation of inflationary responses. While targeting antigen expression to classical hematopoietic antigen presenting cells was insufficient to activate gal-specific CD8+ T cells, expressing the antigen exclusively in CCL19-producing fibroblastic stromal cells (FSCs) induced robust anti-gal CD8+ T cell response. Using bone marrow chimera mice to abolish the expression of major histocompatibility complex I (MHC-I) and Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3) in hematopoietic cells we demonstrated that CCL19-expressing FCS function as antigen libraries, gradually releasing the antigen to CD103+ DCs to maintain gal-specific memory inflating population. Moreover, targeted ablation of CCL19-producing cells revealed that pulmonary fibroblastic stromal cells act as the principal organizer of the nurturing niches that support the metabolic conversion in CD8+ T cells necessary for the generation of long-lasting protective inflationary responses. Overall, our data reveal a hitherto unknown function of CCL19-expressiong fibroblastic stromal in supporting the metabolic fitness of CD8+ T cells, thereby promoting the generation of tissue-specific and long-lasting protective CD8+ T cell responses.

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Transduction of Batf family members provide distinct functions to mouse CD8+ T cells.

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