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Admission CD4+ T cell BTLA expression and its association with infection risk and respiratory outcomes in sepsis.

Created on 18 Aug 2026

Authors

Shuwei Ning, Ying Liu, Changmeng Cao, Ailin Song, Rongxin Sun, Ziqi Rong, Chungang Zhao

Published in

Frontiers in cellular and infection microbiology. Volume 16. Pages 1852916. Epub Aug 03, 2026.

Abstract

T cell co-inhibitory molecule upregulation is linked to sepsis-induced immune suppression, but the relationship between B and T lymphocyte attenuator (BTLA) expression and ICU-acquired infection or organ function recovery in sepsis remains unclear.
This single-center prospective observational cohort study enrolled 143 septic ICU patients. BTLA on CD4+/CD8+ T cells was measured at ICU admission and on days 3/7. Patients were stratified into high- (n=72) and low- (n=71) BTLA-CD4 groups by median baseline CD4+ BTLA level. Primary outcome was ICU-acquired infection developing more than 48 hours after ICU admission. Secondary outcomes included PaO2/FiO2 ratio, ventilator weaning time, 28-day ventilator-free days and 28-day mortality.
The high-expression group had higher ICU-acquired infection (38.9% vs.21.1%, P = 0.033) and 28-day mortality (33.3% vs.9.9%, P = 0.001), but BTLA-CD4 was not an independent predictor for either after multivariable adjustment (infection: OR = 0.937, 95%CI:0.859-1.021, P = 0.139; mortality: HR = 1.034, 95%CI:0.965-1.108, P = 0.342). In a competing-risks analysis accounting for death before weaning, higher BTLA-CD4 was independently associated with delayed ventilator weaning (cause-specific HR = 0.882, 95%CI:0.832-0.936, P<0.001; Fine-Gray subdistribution HR = 0.940, 95%CI:0.902-0.981, P = 0.004). The low-expression group had faster oxygenation recovery and more ventilator-free days (P<0.001).
Elevated CD4+ T cell BTLA expression at ICU admission is independently associated with delayed ventilator weaning in sepsis. Its links to infection and mortality appear to be driven by disease severity. Admission CD4+ T cell BTLA expression may identify a sepsis immune phenotype associated with impaired respiratory recovery, rather than acting as a direct regulator of lung repair.

PMID:
42609383
Bibliographic data and abstract were imported from PubMed on 18 Aug 2026.

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