| Literature DB >> 29602771 |
Julie G Burel1, Cecilia S Lindestam Arlehamn2, Nabeela Khan2, Grégory Seumois2, Jason A Greenbaum2, Randy Taplitz3, Robert H Gilman4,5, Mayuko Saito4,5,6, Pandurangan Vijayanand2, Alessandro Sette2,7, Bjoern Peters2,7.
Abstract
In the context of infectious diseases, cell population transcriptomics are useful to gain mechanistic insight into protective immune responses, which is not possible using traditional whole-blood approaches. In this study, we applied a cell population transcriptomics strategy to sorted memory CD4 T cells to define novel immune signatures of latent tuberculosis infection (LTBI) and gain insight into the phenotype of tuberculosis (TB)-specific CD4 T cells. We found a 74-gene signature that could discriminate between memory CD4 T cells from healthy latently Mycobacterium tuberculosis-infected subjects and noninfected controls. The gene signature presented a significant overlap with the gene signature of the Th1* (CCR6+CXCR3+CCR4-) subset of CD4 T cells, which contains the majority of TB-specific reactivity and is expanded in LTBI. In particular, three Th1* genes (ABCB1, c-KIT, and GPA33) were differentially expressed at the RNA and protein levels in memory CD4 T cells of LTBI subjects compared with controls. The 74-gene signature also highlighted novel phenotypic markers that further defined the CD4 T cell subset containing TB specificity. We found the majority of TB-specific epitope reactivity in the CD62L-GPA33- Th1* subset. Thus, by combining cell population transcriptomics and single-cell protein-profiling techniques, we identified a CD4 T cell immune signature of LTBI that provided novel insights into the phenotype of TB-specific CD4 T cells.Entities:
Mesh:
Year: 2018 PMID: 29602771 PMCID: PMC5991485 DOI: 10.4049/jimmunol.1800118
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422