Epstein Barr Virus Infection Affects Function of Cytotoxic T Lymphocytes in Patients with Severe Aplastic Anemia.
Tian ZhangChunyan LiuHui LiuLijuan LiTing WangRong FuPublished in: BioMed research international (2018)
Severe aplastic anemia (SAA) is characterized by pancytopenia and failure of hematopoietic function and is caused by excessive functioning of cytotoxic T lymphocytes (CTLs). EBNA-1, a nucleoprotein of the Epstein Barr virus (EBV), can influence the proliferation and function of lymphocytes. We therefore tested the number of EBV copies in the CD8+ T cells of 27 patients with SAA and 10 healthy control subjects and observed the influences of EBNA-1 upon the CD8+ T cells of patients with SAA. The results showed that more EBV copies were found in the CD8+ T cells of patients with untreated SAA than in patients with SAA in remission or in the healthy control subjects. Their copy number was positively correlated with the expression of granzyme B and perforin, the secretion level of interferon-γ in CD8+ T cells, and the viability of CD8+ T cells, whereas no correlation was seen between the copy number and the interleukin 4 secretion level or the apoptosis rate. Meanwhile, the expression of granzyme B and perforin was reduced after EBNA-1 gene knockdown, whereas the interferon-γ secretion level and cell viability declined. Therefore, we infer that EBV infection may be a factor in the activation of CTLs and in damaging the bone marrow hematopoietic function of patients with SAA.
Keyphrases
- epstein barr virus
- copy number
- mitochondrial dna
- diffuse large b cell lymphoma
- bone marrow
- genome wide
- poor prognosis
- dna methylation
- chronic kidney disease
- oxidative stress
- allogeneic hematopoietic stem cell transplantation
- cell death
- signaling pathway
- acute lymphoblastic leukemia
- gene expression
- immune response
- long non coding rna
- transcription factor
- body mass index
- iron deficiency
- acute myeloid leukemia