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Expression data from malaria-specific mouse CD4 T cell (PbT-II) subset after Plasmodium chabaudi infection

ABSTRACT: Upon activation, specific CD4+ T cells up-regulate the expression of CD11a and CD49d, surrogate markers of pathogen-specific CD4+ T cells. However, using T-cell receptor transgenic mice specific for a Plasmodium antigen, termed PbT-II, we found that activated CD4+ T cells develop not only to CD11ahiCD49dhi cells, but also to CD11ahiCD49dlo cells during acute Plasmodium infection. CD49dhi PbT-II cells, localized in the red pulp of spleens, expressed transcription factor T-bet and produced IFN-γ, indicating that they were type 1 helper T (Th1)-type cells. In contrast, CD49dlo PbT-II cells resided in the white pulp/marginal zones and were a heterogeneous population, with approximately half of them expressing CXCR5 and a third expressing Bcl-6, a master regulator of follicular helper T (Tfh) cells. In adoptive transfer experiments, both CD49dhi and CD49dlo PbT-II cells differentiated into CD49dhi Th1-type cells after stimulation with antigen-pulsed dendritic cells, while CD49dhi and CD49dlo phenotypes were generally maintained in mice infected with Plasmodium chabaudi. These results suggest that CD49d is expressed on Th1-type Plasmodium-specific CD4+ T cells, which are localized in the red pulp of the spleen, and can be used as a marker of antigen-specific Th1 CD4+ T cells, rather than that of all pathogen-specific CD4+ T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE153600 | GEO | 2021/06/23

REPOSITORIES: GEO

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Project description:Expression data from mouse tumor-specific CD4+ T cells The central role of tumor-specific Th1 cells in fighting cancer is becoming increasingly appreciated. However, little is known about how these cells are generated in vivo. Here, we used flow cytometry and gene expression microarrays to characterize the primary activation and Th1 differentiation of naïve tumor-specific CD4+ T cells in a mouse model for cancer immunosurveillance. We took advantage of T cell receptor-transgenic mice where CD4+ T cells recognize a tumor-specific antigen secreted by the major histocompatibility complex (MHC) class II-negative MOPC315 myeloma. Cancer cells were injected subcutaneously and T cell activation was analyzed in draining lymph nodes and at the incipient tumor site at day +8. After activation and migration to the incipient tumor site, tumor-specific CD4+ T cells had 29 up-regulated molecules (CD2, CD5, CD11a, CD18, CD25, CD28, CD44, CD45, CD49d, CD51, CD54, CD69, CD71, CD83, CD86, CD90, CD95, CD102, CD122, CD153, CD166, CD200, CD249, CD254, CD274, CD279, Ly6C, MHC class I, and CCR7) and 5 down-regulated molecules (CD27, CD31, CD45RB, CD62L, and CD126) on the surface. The activated CD4+ T cells produced interferon , a cytokine consistent with Th1 polarization, and also interleukin 2 (IL-2), IL-3, IL-10, and tumor necrosis factor . Activation of naïve tumor-specific CD4+ T cells in draining lymph node resulted in the up-regulation of 609 genes and down-regulation of 284 genes. Bioinformatics analysis of genes differentially expressed identified functional pathways related to tumor-specific Th1 cell activation. This study may represent a useful resource to guide the development of Th1-based immunotherapy for cancer. TCR-transgenic SCID mice (n = 12-15) were injected s.c. on the flank with 10(5) MOPC315 cells suspended in 250 µl ice-cold growth factor-reduced Matrigel. At day +8, draining axillary LN were dissected out and pooled, single-cell suspensions were made and staining with mAb was carried out. Activated tumor-specific CD4+ GB113+ T cells were sorted by FACSAria (≥ 95% pure) in three independent experiments. Naïve tumor-specific CD4+ control T cells were obtained from pooled LN from naive TCR-transgenic SCID mice and treated identically in two independent experiments.

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Expression data from malaria-specific mouse CD4 T cell (PbT-II) subset after Plasmodium chabaudi infection

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