The Expression Pattern of TCR Vγ I∼III Subfamilies in GVHD Patients After Allogenic Hematopoietic Stem Cell Transplantation.

The γΔ+ T cells can act as a vast functional setting of immune defense against pathogenic invaders in chronic inflammatory reactions, as well as in modulating systemic and organ-specific autoimmune diseases. Recently, it was reported that γΔ+ T cells might play an important role in regulation of graft versus host disease (GVHD), mediation of graft versus leukemia effect, anti-virus infection, anti-cancer effect and so on. But the frequency of T cell receptor (TCR) Vγ repertoire and the expression patterns of TCR Vγ subfamilies in GVHD remain unknown. To further study on the characteristics of TCR Vγ subfamilies in GVHD, we investigated the frequency of TCR Vγ repertoire and the expression of TCR Vγ I∼III subfamilies genes in the patients with GVHD after allogenic hematopoietic stem cell transplantation (allo-HSCT).

The expression and cloanlity analysis of TCR Vγ repertoire was detected in peripheral blood mononuclear cells (PBMNCs) from 25 patients with GVHD by RT-PCR and genescan technique. The TCR Vγ I∼III genes expression levels of PBMNCs from patients with GVHD were detected using the real-time fluorescence quantitative polymerase chain reaction with SYBR Green I technique and relative quantification method. Twelve healthy individuals served as normal controls.

The RT-PCR results showed that in GVHD patients, the expression frequency of TCR Vγ I was 88.0% (22/25), TCR Vγ II was 72.0% (18/25), and TCR Vγ III was 96.0% (24/25). All of the three TCR Vγ subfamilies could be detected in PBMNCs from the normal controls. TCR Vγ repertoires with polyclonal pattern were identified in normal controls. However, the skew expression pattern of TCR Vγ repertoire could be detected in patients with GVHD even more than 4 year after allo-HSCT. Oligoclonal or monoclonal expanded T cells were identified in TCR Vγ I∼III subfamilies in GVHD patients. The expression level of TCR Vγ II gene in the PBMNCs from patients with GVHD was significant lower than the normal controls (P<0.05). The pattern of TCR Vγ gene expression levels in GVHD was TCR Vγ I> TCR Vγ III> TCR Vγ II, however, the expression pattern in normal controls was TCR Vγ II> TCR Vγ I > TCR Vγ III.

The expression patterns of TCR Vγ I∼III subfamilies were changed in GVHD. The low expression of TCR Vγ II subfamily might be related with the pathogenesis of GVHD.

No relevant conflicts of interest to declare.