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Expression of NKG2C and TIGIT on CD56dimCD16+ NK cells in patients with Hemorrhagic fever with renal syndrome

Hemorrhagic fever with renal syndrome (HFRS) is an emerging rodent borne disease caused by negative-sense single-stranded RNA orthohantaviruses (HTV). Clinical characteristics of HFRS infection are acute kidney injury, thrombocytopenia, hemorrhages and hypotension. HTV causes complex immune reactions, which contributes to the pathogenesis. The liver is involved in HFRS pathogenesis, with no enough research evidence about it so far. Natural killer (NK), are found to be activated in HFRS patients. In Cytomegalovirus seropositive HFRS patients, activating receptor NKG2C positive CD56dimCD16+ NK cells were persistently elevated throughout 60 days after onset of symptoms. Our aim was to explore some phenotype changes in NK cells with special focus on TIGIT and NKG2C receptors and their relation to HFRS clinical parameters. We collected blood samples from 15 HFRS patients during early acute (upon hospital admission) and late acute (at discharge) stage of disease, and 9 healthy controls. Using flow cytometry we analysed CD56dimCD16+ NK cells. We observed higher percentage of this population in patients with severe clinical picture compared to patients with mild disease. In addition, percentage of NKG2C positive cells was positively correlated with percentage of inhibitory receptor TIGIT positive cells during the early stage of disease. Interestingly, low percentage of both parameters were detected in patients with hepatomegaly and significantly high percentage in patients with no hepatomegaly. Our results suggest possible important role of NK cells driven immune reaction in liver in HFRS patients and special research focus should be directed to the liver involvement in HFRS pathogenesis in the future

Hemorrhagic fever with renal syndrome

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