Immune checkpoint blockade (ICB) has transformed cancer treatment, yet durable responses are limited. The co-occurrence of B cells and CD8⁺ T cells within tertiary lymphoid structures (TLS) correlates with prognosis and ICB responses. Here, we investigate if engaging co-stimulatory pathways, specifically agonism of glucocorticoid-induced TNFR-related protein (GITR), can simultaneously enhance B cell and T cell anti-tumor responses to improve ICB efficacy. In ICB-refractory advanced melanoma and pancreatic ductal adenocarcinoma (PDAC) models, GITR agonism (GITRa) drives robust B cell activation, promoting germinal center formation, somatic hypermutation, and BCR repertoire diversification. Mechanistically, GITRa reduces Tfr-mediated suppression and enhances Tfh-derived cytokines, supporting antibody class switching and tumor-specific IgG1 responses. Despite these effects, GITRa alone does not control tumors and induces a dysfunctional CD8⁺ T cell state marked by PD-1 and LAG-3 upregulation. However, combining GITRa with dual PD-1/LAG-3 blockade improves tumor control and survival, reduces CD8+ T cell dysfunction and increases B cells and TLS formation, particularly in PDAC. B cell depletion partially impairs efficacy, underscoring their role in tumor control. Together, these findings position clinically translatable GITRa as an approach that mobilizes both cellular and humoral anti-tumor immunity, promotes TLS formation, and sensitizes ICB-resistant melanoma and PDAC to ICB.