# Association between immune cells and allergic purpura: a Mendelian randomization study

## TL;DR

This study uses genetic data to find a potential causal link between specific immune cell markers and the risk of allergic purpura.

## Contribution

The study identifies two immune cell markers with a causal effect on allergic purpura using Mendelian randomization.

## Key findings

- HLA-DR on CD14+CD16- monocytes is associated with increased allergic purpura risk (OR: 1.2379).
- CD11b on basophils is linked to higher allergic purpura risk (OR: 1.2973).
- Sensitivity analyses confirmed the robustness of these associations.

## Abstract

Increasing evidence indicates a substantial correlation between the immune cells and the risk of allergic purpura. We utilized Mendelian randomization (MR) to investigate causal effect of immune cell on allergic purpura.

Genetic instrumental variables for immune cells were sourced from an extensive genome-wide association study (GWAS) comprising 3757 participants. Summary statistics of allergic purpura, involving 470 cases and 216,099 controls, were obtained from FinnGen. The primary analysis employed the inverse-variance weighted (IVW) method. Rigorous sensitivity analyses including MR-Egger, weighted median and MR-PRESSO were conducted to ensure the reliability of the causal estimate.

We identified two immunophenotypes associated with an increased risk of allergic purpura: HLA-DR on CD14 + CD16- monocyte (OR: 1.2379; 95% CI: 1.0612–1.4440; P = 0.0066) and CD11b on basophil (OR: 1.2973; 95% CI: 1.0905–1.5433; P = 0.0033). The sensitivity analyses consistently yielded similar results for these immunophenotypes.

Our analyses confirmed a potential causal effect of HLA-DR on CD14 + CD16- monocyte, as well as CD11b on basophils, in relation to the risk of allergic purpura. Further studies are necessary to clarify the mechanisms by which these immunophenotypes influence the development of allergic purpura.

The online version contains supplementary material available at 10.1186/s13052-025-01847-6.