Panniculitis, characterized by inflammation of the subcutaneous adipose tissue, displays diverse clinical and dermatohistopathological phenotypes. However, the underlying pathomechanisms remain largely unknown, with limited studies pointing to a delayed-type III/IV hypersensitivity reaction. In the present study, we aimed to gain new insights into the pathogenesis of the two most common panniculitis subtypes, erythema nodosum (EN) and erythema induratum (EI), by exploring their cellular and molecular immune patterns. We analyzed deep lesional skin biopsies from EN and EI patients (n=16 per group) and healthy controls (n=6) using imaging mass cytometry (IMC) to map the leukocytic infiltrate. The IMC analysis revealed distinct cellular profiles for EN and EI. In both conditions, macrophages were the predominant immune cell type, exhibiting a shift towards an M1 phenotype compared to healthy controls. In EI, the M1 macrophages were particularly prominent and were noted to cluster with activated CD8+ T cells. Conversely, EN showed fewer inflammatory features and a larger B cell population. These cellular changes were supported by an overall strong type 1 immune signature on the mRNA level in both EN and EI. This was evidenced by the upregulation of NLR-, NFkB-, and inflammasome-signaling-pathway genes compared to healthy controls. The type 1 signature was more pronounced in EI than in EN. These findings challenge the current understanding of panniculitis. They point towards a key role of M1 macrophages in mediating both innate and adaptive immune responses in panniculitis.