1Mahmood Hachim,2Ibrahim Hachim, 3Suad Hannawi
1Clinical Sciences Department, College Of Medicine, University Of Sharjah, 2University of Sharjah, 3Ministry of Health and Prevention (MOHAP)
Background:
Memory T cells (TM) cells are T cells with more prolonged survival and faster recall responses upon secondary challenge. Effector memory-T subset was shown to be explicitly expanded in the peripheral blood of patients with RA in correlation with disease activity[1]. Their disturbance was reported in early RA with intrinsic abnormalities in differentiating into cytokine-producing effector cells[2]. The molecular basis of such abnormalities is not yet known.
Using publically available transcriptomic database to explore transcriptomic profiling of naïve, central memory, effector memory cells, and stem cell the least-developed memory subset memory T cells of human CD4+ T cells from patients with rheumatoid arthritis to identify biomarkers that can indicate their activation.
Material(s) and Method(s):
Methodology
A recently publicly available transcriptomic dataset (GSE80785) was identified using GEO Omnibus database (https://www.ncbi.nlm.nih.gov/geo/) that fulfills the criteria of cells examined. GEO2R tool (https://www.ncbi.nlm.nih.gov/geo/geo2r/?acc=GSE80785) was used to identify common DEGs between the different groups.
Result(s):
Three genes (KLRB1, CD58, and FAM129A) were found to be unique markers for developed (central and effector) memory T cells in Rheumatoid arthritis compared to naïve and stem cell least-developed memory subset memory T cells with the highest expression in effector ones. Their expression was increasing with the memory status of the CD4 cells indicating their role in memory and making them potential biomarkers for activated autoreactive T cells in RA
Conclusion(s):
KLRB1, CD58, and FAM129A are unique markers for developed (central and effector) memory T cells in Rheumatoid arthritis