Tumour immunology articles from across Nature Portfolio

In a mouse model of lymphoma, inflammasome dysfunction increases hematopoietic stem cell turnover and accelerates lymphomagenesis. Our data show that inflammasome function, through the NLRP3–ASC–caspase 1–GSDMD axis, in bone marrow stromal cells controls the rate of hematopoietic stem cell proliferation and thereby reduces premalignant to malignant transformation.

It has been previously reported that the natural cytotoxic receptor NKp46 plays an important role in regulating natural killer (NK) cell biology. Here the authors show that NKp46 is required for the proliferation and cytotoxicity of type 1 innate lymphoid cells (ILCs) by activating the NF-κB signaling pathway and regulating IL-2Rα expression.

In a mouse model of lymphoma, inflammasome dysfunction increases hematopoietic stem cell turnover and accelerates lymphomagenesis. Our data show that inflammasome function, through the NLRP3–ASC–caspase 1–GSDMD axis, in bone marrow stromal cells controls the rate of hematopoietic stem cell proliferation and thereby reduces premalignant to malignant transformation.

Leptomeningeal metastases of solid tumors are associated with poor prognosis, limited treatment options and unclear immunosurveillance mechanisms. Dura-derived immunosuppressive macrophages are now shown to migrate to the cerebrospinal fluid, limiting anti-tumor CD8⁺ T cell responses in models of leptomeningeal metastasis.

In 2024, two groundbreaking approvals from the US Food and Drug Administration for T cell-based therapies that target solid tumors were achieved. Lifileucel, a polyclonal tumor-infiltrating lymphocyte-based product for melanoma, and afamitresgene autoleucel, a gene-engineered T cell receptor product for sarcoma, mark a major shift from the six chimeric antigen receptor T cell therapies previously approved for hematological malignancies.

By tracking the fate of tumor-specific T cells mobilized in lymph nodes by dual blockade of PD-1 and TIGIT, we show that both exhausted T cells and effector T cells can emerge from a common progenitor. Signaling by the co-stimulatory receptors CD28 and CD226 is important for deciding between these two cell fates.