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Authors: Lei Lei1 et al. Link to paper:

Journal/ Pre-Print: medRxiv and bioRxiv

Key Words: γδ T cells, COVID-19, CD25, Biomarker

Research Highlights

1. γδ T cells are decreased in COVID-19 patients

2. Percentage of γδ T cells expressing CD4 is increased in COVID-19 patients

3. The activation marker CD25 is increased in γδ T cells of COVID-19 patients


This study contributes to immunological characteristics of COVID-19 by investigated changes in γδ T cells number and phenotype. Normally, γδ T cells number increases in the early stage of vital infections while in COVID-19 patient the number of γδ T cells was decreased. γδ T cells did show a more activated phenotype by an increased expression of CD25. γδ T cells which normally show a predominately CD4/CD8 double negative phenotype, displayed an increased expression of CD4 on their surface in COVID-19 patients compared to Healthy controls which could be used as a biomarker to indicate COVID-19 infection.

Impact for SARS-CoV2/COVID19 research efforts

Understand the immune response to SARS-CoV2/COVID19: Study shows a decrease of γδ T cells with an increased activated phenotype which contributes to the understanding of the immune response.

Study Type

· Patient Case study

Strengths and limitations of the paper

Novelty: The new insight from this paper is that γδ T cells are decreased and show a more CD4 and activated phenotype.

Standing in the field: The reported results are not controversial, previous studies found lymphopenia and an increase of CD4 phenotype. In this study they found the same pattern in a specific T-cell subset.

Appropriate statistics: The study uses two groups: COVID-19 n=38 vs HD n=18, and used student t-test for statistical analysis. Statistical analysis should probably have used Mann Whitney U test.

Viral model used: Analysis is on patients infected with SARS-CoV2

Translatability: Study is a limited preliminary observational study on the frequency of γδ T cells in circulation.

Main limitations: Study only investigated one type of immune cell (γδ T cells) and also failed to investigate the different subsets of this immune population. In addition, the same authors have submitted an additional paper that appears to use the same cohort of PBMC samples and details the results

of other immune subsets such CD4+ T cells, CD8+ T cells and B cells (

This paper is weakened by splitting this data across two manuscripts – the additional manuscript has been previously reviewed and the same limitations outlined in that review apply here. Additionally, the patient samples that were used in this study were positive-tested for Covid-19 but there is no accompanying patient details for the cohort used – the previous reviewed manuscript mentioned above using this same PBMC cohort noted that these patient details are also missing in that manuscript (they refer to a table 1 in previous manuscript which is absent). Labelling of plots in Figure 2 is incorrect – CD25 is shown on two plots.