Interpreting immunoregulation in lung fibrosis: a new branch of the immune model.
(2024) Resolution of Pulmonary Fibrosis — Location: Orléans, France (10.June.2024)
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- Abstract
- Immunostimulation is recognized as a significant contributor to lung fibrosis in certain animal models and subsets of patients. Recently, we have elucidated an additional mechanism involving the potential implication of immunoregulation during fibrogenesis. Both animal and human data suggest that pulmonary fibrosis encompasses distinct immunoregulatory populations, including regulatory lymphocytes (T and B regs) and myeloid cells (immunosuppressive macrophages and myeloid-derived suppressor cells; MDSCs). Initially recruited to mitigate harmful inflammation, these cells also play a role in the development of lung fibrosis by secreting immunoregulatory mediators (primarily TGF-β1 and IL-10) that directly or indirectly stimulate fibroblasts and promote matrix protein deposition. The presence of this silent immunoregulatory environment supports an alternative mechanism of fibrosis, which explains why deficiencies in pro-inflammatory cytokines or treatments with steroids or immunosuppressants do not always effectively mitigate lung fibrosis under certain conditions. The sustained presence of immunoregulation is a critical consideration for refining therapeutic strategies in lung fibrotic disorders, particularly in non-inflammatory environments.
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Huaux, F. (2024). Interpreting immunoregulation in lung fibrosis: a new branch of the immune model. Resolution of Pulmonary Fibrosis, Orléans, France. https://hdl.handle.net/2078.5/239273