• Daithi S Heffernan, Sean F Monaghan, Chun-Shiang Chung, William G Cioffi, Stefan Gravenstein, and Alfred Ayala.
• Division of Surgical Research, Department of Surgery, Warren Alpert Medical School of Brown University, Rhode Island Hospital, Providence, RI 02903, United States. Electronic address: dheffernan@brown.edu.
• Hum. Immunol. 2014 Mar 1; 75 (3): 277-82.

BackgroundSepsis is associated with severe immunosuppression, evidenced by loss and dysfunction of CD3(+) lymphocytes and γδ-TCR(+) T-cells. There is limited data addressing changes in the invariant natural killer T-(iNKT) cell population with sepsis, and whether such changes correlate with clinical outcomes. Specifically, septic geriatric patients have marked mortality. How γδ-TCR(+) T-cells and iNKT-cells are altered in the settings of sepsis and advanced age, and how these changes correlate with mortality are unknown.Methods49 young (18-50years) and 55 geriatric (>65years) ICU patients with confirmed sepsis were enrolled. Blood was stained with antibodies to detect the percentage and absolute number of CD3(+) (T-cells), γδ-TCR(+) T-cell, TCR-Vα-24(+) (iNKT-cells), and CD69(+) (marker of cell activation). Blood from 10 healthy controls was also collected.ResultsSeptic patients displayed marked leukocytosis, decreased CD3(+) lymphocytes, and γδ-TCR(+) T-cells, and increased percentage and number of iNKT-cells. Young and geriatric patients had similar degree of leukocytosis, along with percentage, number, and %CD69(+) CD3(+) T-cell and γδ-TCR(+) T-cells; however, percentage, number, and %CD69(+)iNKT-cells were most markedly elevated in geriatric patients. Geriatric non-survivors had higher percentage and number of, but decreased %CD69(+), iNKT-cells vs survivors.ConclusionsiNKT-cells are increased in sepsis, suggesting that they typify an evolving morbid state. This is most pronounced in geriatric non-survivors, a group demonstrating dysfunctional regulatory iNKT-cell phenotype.Copyright © 2013 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

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