Hashimoto’s thyroiditis (HT) and differentiated thyroid cancer (DTC) frequently coexist, yet their biological relationship remains paradoxical. In this critical narrative review informed by a structured literature search, we synthesize epidemiological, clinicopathological, genomic, immunological, and translational evidence derived predominantly from papillary thyroid carcinoma (PTC) within the broader DTC framework to examine how HT may function as both a tumor-promoting inflammatory niche and a tumor-restraining immune microenvironment. In the proposed spear-and-shield model, chronic autoimmune inflammation may generate oxidative stress, cytokine signaling, and selective pressures that favor malignant transformation, whereas pre-existing lymphocytic infiltration, antigen presentation, B-cell organization, and cytotoxic T-cell activity may strengthen immune surveillance and contribute to favorable outcomes in selected patients. We further discuss how immune escape can emerge within an inflamed thyroid microenvironment through checkpoint activation, regulatory lymphocytes, myeloid polarization, dendritic-cell remodeling, and thyroid-stimulating hormone/thyroid-stimulating hormone receptor (TSH/TSHR)-related immune modulation. Finally, because most mechanistic and clinical evidence derives from papillary thyroid carcinoma, we emphasize that HT should be characterized according to its timing, histological features, antibody profile, thyroid functional status, and spatial immune organization. We propose that HT influences DTC through a stage- and genotype-dependent immune contexture rather than as a uniform risk factor, and identify testable biomarkers integrating T-cell and B-cell receptor clonality, tertiary lymphoid structure maturity, antigen presentation, checkpoint activation, thyroid differentiation, and TSH–TSHR signaling.