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Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is characterized by progressive tissue remodeling and extracellular matrix deposition, yet the cellular and molecular mechanisms that drive persistent fibrosis remain incompletely understood. Increasing evidence suggests that fibrosis is not simply the consequence of aberrant fibroblast activation, but emerges from complex interactions among stromal cells, immune populations, and the extracellular matrix.

In this seminar, I will discuss the role of fibroblast–immune crosstalk in shaping the fibrotic lung microenvironment, with particular emphasis on laminin α4 (LAMA4) and its potential role in regulating interactions between fibroblasts and natural killer (NK) cells. We will explore how changes in extracellular matrix composition may influence immune cell localization and function, and how NK cell–fibroblast interactions may contribute to the persistence or resolution of fibrosis.

By examining these interconnected cellular and molecular pathways, this seminar will highlight the emerging role of the extracellular matrix as an active regulator of immune responses and discuss how a better understanding of fibroblast–immune interactions may reveal new therapeutic strategies for SSc-ILD.