AUTHOR=Wong Connie H. Y. , Jenne Craig N. , Tam Patrick P. , Léger Caroline , Venegas Andres , Ryckborst Karla , Hill Michael D. , Kubes Paul 

TITLE=Prolonged Activation of Invariant Natural Killer T Cells and TH2-Skewed Immunity in Stroke Patients

JOURNAL=Frontiers in Neurology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00006

DOI=10.3389/fneur.2017.00006

ISSN=1664-2295

ABSTRACT=<sec id="ST1"><title>Background</title><p>Infection is highly prevalent and contribute significantly to mortality of stroke patients. In addition to the well described robust systemic lymphocytopenia and skewed T helper 2 (T<sub>H</sub>2)-immunity after stroke, emerging experimental evidence demonstrate that the development of infection poststroke is attributed by the activation of invariant natural killer T (<italic>i</italic>NKT) cells. In this prospective study, we examined the levels of a broad spectrum of inflammatory mediators, the activation status of <italic>i</italic>NKT cell in the blood of patients with various degree of stroke severity, and investigate whether these parameters differ in patients who later develop poststroke infections.</p></sec><sec id="ST2"><title>Methods and results</title><p>We obtained blood from stroke patients and matching controls to perform flow cytometry and multiplex measurement of inflammatory mediators. Our data suggest a pronounced activation of <italic>i</italic>NKT cells in stroke patients as compared with matched Healthy and Hospital control patients. The magnitude of <italic>i</italic>NKT activation is positively correlated with the severity of stroke, supporting the hypothesis that <italic>i</italic>NKT cells may contribute in the modulation of the host immune response after stroke-associated brain injury. In addition, stroke severity is closely correlated with decreased T<sub>H</sub>1/T<sub>H</sub>2 ratio, increased production of interleukin (IL)-10, with infected stroke patients showing exacerbated production of IL-10.</p></sec><sec id="ST3"><title>Conclusion</title><p>Stroke triggers a robust and sustained shift in systemic immunity in patients, including specific lymphopenia, robust activation of <italic>i</italic>NKT cells, systemic production of IL-10, and a prolonged T<sub>H</sub>2-skewed immunity, all are potential contributors to severe immune suppression seen in patients after stroke. Future studies with large sample size will provide potential causality relationship insights.</p></sec>