Luminal B breast cancer (LBBC) represents an aggressive, high-grade ER+ disease, associated with a high proliferation rate, higher mutation burden, and higher probability of eliciting the immune response. Clinical and pathological data from 89 patients of stage II-III, triple-negative (TN), and luminal B-like BC (LB-like BC) were included in the analysis. All patients were submitted to neoadjuvant chemotherapy (NACT). Quantitative and qualitative evaluations of TILs (Tumor-Infiltrating Lymphocytes) were performed on tissue microarrays constructed from pretreatment core-needle biopsy tumor specimens. The proportion of stromal TILs, CD8, CD4, and PD-L1 positive (+) immune cells (IC), as well as the number of FOXP3, CTLA4, and HSP-70+ IC, was observed concerning tumor immunophenotype, traditional clinicopathological prognostic factors, and tumor response to NACT. There was no statistically significant difference in the proportion of stromal TILs between the LB-like and TNBC (p = 0.344) cohorts. However, a higher CD4/CD8 ratio was associated with the TNBC biology (p = 0.018) and within the LB-like BC cohort with a high proliferation index and metastatic nodal involvement (p = 0.045, p = 0.015). Within the LB-like BC cohort, a higher expression of PD-L1 and HSP70+ IC was associated with a high proliferation index of tumor cells (p = 0.018, p = 0.040), massive metastatic nodal involvement (p = 0.002, p = 0.026), and higher stages of disease (p = 0.004, p = 0.042). Better response to NACT was associated with higher numbers of HSP70+ IC and higher proportions of CD8+ cells within the LB-like BC cohort (p = 0.045, p = 0.012). Routine evaluation of immune markers and HSP70 may help identify high-risk patients of LB-like breast cancer who would have a better response to NACT.

Background/Objectives: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by dysregulated immune responses. This study aimed to assess the expression of IL-1β, IL-8, IL-10, and TNF-α in HS lesioned and non-lesioned skin and to examine their associations with selected clinical characteristics. Methods: Skin samples from HS lesions and non-lesioned skin were obtained from 52 patients. Histopathological changes were assessed using hematoxylin and eosin staining, and cytokine expression was evaluated by immunohistochemistry and quantified using ImageJ. Cytokine expression was analyzed according to Hurley stage and selected demographic and clinical characteristics. Results: Of 52 patients, 24 (46%) were female. Patient’s median age was 35.5 (IQR 26-44) years; 28 (54%) patients were categorized as Hurley stage 2 and 24 (46%) as stage 3. IL-1β, IL-8, IL-10, and TNF-α expression was significantly higher in lesioned than in non-lesioned skin (all p<0.05). IL-1β expression was higher in Hurley stage 2 than stage 3 (p=0.042), whereas IL-8 expression was higher in Hurley stage 3 (p=0.039). No significant differences were found according to sex, BMI, smoking, or biological therapy. TNF-α expression was significantly higher in patients with a positive family history of HS (p=0.049). Conclusions: HS lesions demonstrate increased expression of both pro-inflammatory and regulatory cytokines. Differences in IL-1β and IL-8 expression across Hurley stages suggest that inflammatory pathways may vary with disease stage. The association between TNF-α expression and positive family history may indicate a potential genetic influence on the inflammatory phenotype of HS.