Autologous stem cell transplantation (SCT) remains an important consolidation treatment for patients with multiple myeloma (MM) and is thought to prolong disease plateau-phase by providing intensive cytoreduction. However, SCT also induces inflammation in the context of profound lymphodepletion that may result in hitherto unexpected immunological effects. We developed a preclinical model of SCT for MM using Vk*MYC myeloma that recapitulates clinical disease. Surprisingly, we demonstrate the induction of T cell-dependent myeloma control after SCT as survival was prolonged in recipients of bone marrow (BM) grafts containing T cells compared to BM alone (BM+T cells vs. BM; median survival 106 vs. 58 days, p=0.0001). This anti-myeloma activity was independent of gamma-delta T, natural killer (NK) T and NK cells. TCR sequencing of CD8⁺ T cells from mice with controlled myeloma revealed a distinct repertoire structure and higher clonotype overlap relative to myeloma-free SCT recipients, consistent with the induction of myeloma-specific T cells. Furthermore, T cell-dependent myeloma control could be adoptively transferred to secondary recipients and was myeloma clone-specific. Interestingly, lack of donor-derived IL-17A prolonged survival (WT vs. IL-17A^–/–donor; median survival 67 days vs. unreached at 120 days, p=0.0007). IL-17A acted directly on myeloma cells expressing the IL-17-receptor to induce a transcriptional landscape that promoted tumor growth and immune escape. Conversely, donor IFNγ secretion and signalling was critical to protective immunity and CD8⁺ T cells from mice with relapsed myeloma had impaired IFNγ production compared to those with controlled disease. Importantly, IFNγ production was profoundly augmented by the administration of a CD137 agonist such that the majority of mice were cured. This provides new insights into the mechanisms of action of SCT in myeloma and suggests rational approaches to improving clinical outcome.