Abstract
Little is known of the adaptive immune response to subarachnoid hemorrhage (SAH). This study was the first to investigate whether T cell receptor (TCR) immune repertoire may provide a better understanding of T cell immunology in delayed cerebral ischemia (DCI). We serially collected peripheral blood in five SAH patients with DCI. High-throughput sequencing was used to analyze the TCR β chain (TCRB) complimentary determining regions (CDR) 3 repertoire. We evaluated the compositions and variations of the repertoire between admission and the DCI period, for severe DCI and non-severe DCI patients. Clonality did not differ significantly between admission and DCI. Severe DCI patients had significantly lower clonality than non-severe DCI patients (p value = 0.019). A read frequency of 0.005% ≤ – < 0.05% dominated the clonal expansion in non-severe DCI patients. Regarding repertoire diversity, severe DCI had a higher diversity score on admission than non-severe DCI. The CDR3 lengths were similar between admission and DCI. Among 728 annotated V-J gene pairs, we found that the relative frequencies of two V-J pairs were different at the occurrence of DCI than at admission, with T cells increasing by over 15%. TCRB CDR3 repertoires may serve as biomarkers to identify severe DCI patients.
Highlights
T cells are categorized into two groups according to the T cell receptor (TCR) expressing either α and β chains or γ and δ chains [1], and approximately 90% to 95% of the T cells in peripheral blood encode α and β chains
Li et al [1] reported that patients with acute myocardial infarction (AMI) exhibited specific CDR3 amino acids and reconstituted TCR immune repertoires
We sequenced TCR β-chain (TCRB) CDR3 repertoires from the five subarachnoid hemorrhage (SAH) patients treated with coil embolization and compared repertoires between the different day of admission and delayed cerebral ischemia (DCI) development, as well as between severe and non-severe DCI patients
Summary
T cells are categorized into two groups according to the T cell receptor (TCR) expressing either α and β chains or γ and δ chains [1], and approximately 90% to 95% of the T cells in peripheral blood encode α and β chains. CDR3 is the most variable of the regions, and it associated with the antigen-binding specificity of TCRs [2]. CDR3 exhibits unique TCRs through a random somatic recombination of the Variable (V), Diversity (D) and Joining (J) gene segments [1]. Over the past few years, TCR sequencing has been performed to identify immune T-cell signatures for various diseases, such as immune disease or cancer immunotherapy [3,4], suggesting the specific TCR repertoire plays a possible role as markers monitoring the immune status or treatment response [2]. In addition to immune diseases, TCR sequencing may monitor the cardiovascular-immune microenvironment and disease pathogenesis [1]. Li et al [1] reported that patients with acute myocardial infarction (AMI) exhibited specific CDR3 amino acids and reconstituted TCR immune repertoires
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