TRIM28 Promotes Keratinocyte Proliferation and Invasion by Activating NLRP3/SGT1 Axis‐Mediated Macrophage Pro‐Inflammatory Polarization in an In Vitro Macrophage–Keratinocyte Co‐Culture Model

Abstract

Macrophage–keratinocyte crosstalk is an important component of cutaneous inflammatory responses. Psoriasis is a chronic inflammatory skin disease characterized by dysregulated keratinocyte proliferation and immune dysfunction. While macrophage pro‐inflammatory activation is known to exacerbate psoriatic inflammation, the underlying molecular mechanisms remain incompletely understood. TRIM28, a multifunctional regulatory protein, may play a role in this process, but whether TRIM28 regulates macrophage–keratinocyte crosstalk in a psoriasis‐relevant inflammatory context remains unclear. The present study was designed as an in vitro mechanistic investigation and does not establish TRIM28 dysregulation in human psoriasis. Therefore, psoriasis is discussed only as a potential disease context, rather than as a conclusion directly supported by the present data.