# Platelet-Sourced TGF-β Promotes Th17 Responses and Enhances Airway Neutrophilia

## TL;DR

This study shows that platelets help Th17 cells grow in the lungs, worsening asthma symptoms caused by fungi like Candida.

## Contribution

The paper reveals a novel role of platelet-sourced TGF-β in promoting Th17 responses in fungal-induced asthma.

## Key findings

- C. albicans induces platelet infiltration into the lungs.
- Platelet TGF-β activates and supports Th17 cells, increasing airway neutrophils.
- Platelet transfer worsens Th17-driven inflammation in asthma models.

## Abstract

Microbial, especially fungal, sensitization has been associated with the development and exacerbation of treatment-refractory neutrophilic asthma. Among the airway-inhabiting fungi, Aspergillus fumigatus and Candida albicans are the dominant species that elicit protective T helper (Th) 17 and other T cell responses, contributing to airway neutrophilia and steroid resistance. However, it is not fully understood how fungal airway colonization impacts the immunopathogenesis of asthma. Here, we used a neutrophilic asthma model induced by C. albicans to study the immune regulation of this disease. We found that intranasal administration of C. albicans induced platelet infiltration into the lung. Platelet-expressed latent TGF-β could be activated specifically by Th17 cells and drive the commitment, maintenance, and expansion of Th17 cells. In Candida-induced asthma, an adoptive transfer of platelets enhanced Th17 responses, increasing airway neutrophil influx. Thus, managing airway mycobiota and reducing platelet intrapulmonary infiltration may serve as a promising interventional approach.