Fibrosis is a common final outcome of most chronic inflammatory diseases, especially chronic lung diseases. Fibrosis impacts organ function and ultimately leads to organ failure and death. To date, as many as 45% of all deaths in the developed world are related to pathological tissue remodeling. Chronic lung diseases (CLD) are the 3rd leading cause of death worldwide. The availability of effective therapies and biomarkers for individualized diagnosis, monitoring, and therapy is, however, highly limited. Among CLD, Idiopathic Pulmonary Fibrosis (IPF) is a chronic and lethal fibroproliferative disease of the lung, with unknown etiology. IPF is characterized by progressive fibrosis and irreversible loss of lung function, with a median survival, or time to lung transplantation, of about 3 years after diagnosis. In many organs, innate and adaptive immunity contributes to fibrogenesis. Rising evidence shows that abnormal immune responses are implicated in IPF pathophysiology.

 Our scientific focus is to understand the contribution of the immune system to organ fibrosis.


‘Immune networks in chronic lung diseases’

Projects details:

·       Functional assessment of interactions between mononuclear myeloid cells and lung structural cells.

·       Identification of key ligand/receptor interactions in immune-structural lung cell crosstalk

·       Molecular characterization of in immune-structural lung cell interaction

·       Target evaluation in in-vitro models

Source: Isis E. Buelvas Fernandez, Helmholtz Zentrum München, ILBD/CPC

‘Biomarker discovery in pulmonary fibrosis’

Projects details:

·       Multi-compartmental biomarker discovery in chronic lung diseases.

·       Flow cytometry based peripheral blood immunophenotyping of chronic lung disease patients.

·       Identification of key immune cell populations in perpetuation of fibrosis.



 Source: Isis E. Buelvas Fernandez, modified after Greiffo FR, Helmholtz Zentrum München, ILBD/CPC