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Both percentage of γδ T lymphocytes and CD3 expression are reduced during septic shock

Venet, Fabienne MSc; Bohé, Julien MD, PhD; Debard, Anne-Lise Pharm D; Bienvenu, Jacques Pharm D, PhD; Lepape, Alain MD; Monneret, Guillaume PharmD, PhD

doi: 10.1097/01.CCM.0000189745.66585.AE
Brief Reports

Objective: The mechanisms involved during sepsis-induced immunosuppression are far from being extensively established. The objective of the present study was to investigate whether two characteristics of T cells were altered in this situation: the percentage of circulating γδ T lymphocytes and the level of CD3 expression on T lymphocytes.

Design: Observational study.

Setting: Adult intensive care units in a university hospital.

Patients: Patients with septic shock (n = 21) and healthy individuals (n = 21).

Interventions: None.

Measurements and Main Results: In patients, we first observed the decreased percentage of γδ T lymphocytes in peripheral blood (1% [0.7–3.1], median [interquartile range]) in comparison with healthy individuals (3.5% [2.1–4.8]). Regarding CD3, we measured a highly significant decrease of its expression on both αβ and γδ T lymphocytes from patients (p < .005), whereas the CD3 mean fluorescence intensities ratio (γδ/αβ) was not affected: 2.2 [2.1–2.4] and 2.1 [1.9–2.3] in healthy individuals and septic patients, respectively. The magnitude in the decrease of CD3 expression was thus similar in αβ and γδ cells, suggesting a common down-regulation mechanism for both T-cell lineages.

Conclusions: Combined with a reduced percentage of monocytes expressing human leukocyte antigen-DR, a reduced CD3 expression may be involved in the failure of antigen presentation depicted after septic shock, whereas the diminished percentage of circulating γδ T cells could be partly responsible for the elevated incidence of secondary infections. These two observations constitute additional pieces of the complex puzzle of sepsis-induced immunosuppression.

From Immunology Laboratory (FV, ALD, JBi, GM) and Intensive Care Units (JBo, AL), Lyon-Sud University Hospital, France; and Immunology Laboratory (GM), Hôpital Neurologique, Lyon, France.

None of the authors has any potential financial conflict of interest related to this manuscript.

© 2005 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins