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Patients with cystic fibrosis, chronic obstructive pulmonary disease, severe asthma, pre-existing pulmonary lesions, and severely immunocompromised patients are susceptible to develop infections with the opportunistic pathogenic fungus  Aspergillus fumigatus , called aspergillosis. Infections in these patients are associated with persistent pro-inflammatory T-helper (T H )2 and T H 17 responses. Regulatory T-cells, natural suppressor cells of the immune system, control pro-inflammatory T-cell responses, but can also contribute to disease by shifting to a pro-inflammatory T H 17-like phenotype. Such a shift could play an important role in the detrimental immunopathology that is seen in aspergillosis. Our study demonstrates that  Aspergillus fumigatus  induces regulatory T-cells with a T H 17-like phenotype. We also demonstrate that these regulatory T-cells with a pro-inflammatory T H 17-like phenotype can be reprogrammed to their “classical” anti-inflammatory phenotype by activating Toll-like receptor 2 (TLR2), which regulates the induction of cytotoxic T-lymphocyte-associated protein 4 (CTLA4). Similarly, soluble CTLA4 could reverse the pro-inflammatory phenotype of  Aspergillus- induced regulatory T-cells. In conclusion, our results suggest a role for regulatory T-cells with a pro-inflammatory T H 17-like phenotype in  Aspergillus -associated immunopathology, and identifies key players, i.e. TLR2 and CTLA4, involved in this mechanism.

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Toll-like receptor 2 induced cytotoxic T-lymphocyte-associated protein 4 regulates Aspergillus-induced regulatory T-cells with pro-inflammatory characteristics