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Alspach, E.

Publications and source records attributed to Alspach, E..

2 recordsLinked to original sources

Overlapping and Distinct Mechanisms of Effective Neoantigen Cancer Vaccines and Immune Checkpoint Therapy

The goal of therapeutic cancer vaccines and immune checkpoint therapy (ICT) is to eliminate cancer by expanding and/or sustaining T cells with anti-tumor capabilities. However, whether cancer vaccines and ICT enhance anti-tumor immunity by distinct or overlapping mechanisms remains unclear. Here, we compared effective therapeutic tumor-specific mutant neoantigen (NeoAg) cancer vaccines with anti-CTLA-4 and/or anti-PD-1 ICT in preclinical models. Both NeoAg vaccines and ICT induce expansion of intratumoral NeoAg-specific CD8 T cells, though the degree of expansion and acquisition of effector activity was much more substantial following NeoAg vaccination. Further, we found that NeoAg vaccines are particularly adept at inducing proliferating and stem-like NeoAg-specific CD8 T cells. Single cell T cell receptor (TCR) sequencing revealed that TCR clonotype expansion and diversity of NeoAg-specific CD8 T cells relates to their phenotype and functional state associated with specific immunotherapies employed. Effective NeoAg vaccines and ICT required both CD8 and CD4 T cells. While NeoAg vaccines and anti-PD-1 affected the CD4 T cell compartment, it was to less of an extent than observed with anti-CTLA-4, which notably induced ICOS+Bhlhe40+ Th1-like CD4 T cells and, when combined with anti-PD-1, a small subset of Th2-like CD4 T cells. Although effective NeoAg vaccines or ICT expanded intratumoral M1-like iNOS+ macrophages, NeoAg vaccines expanded rather than suppressed (as observed with ICT) M2-like CX3CR1+CD206+ macrophages, associated with the vaccine adjuvant. Further, combining NeoAg vaccination with ICT induced superior efficacy compared to either therapy in isolation, highlighting the utility of combining these modalities to eliminate cancer. HighlightsO_LINeoAg cancer vaccines utilize distinct mechanisms from CTLA-4 or PD-1 ICT C_LIO_LINeoAg vaccines induce TCF1+ stem-like and proliferating NeoAg-specific CD8 T cells C_LIO_LICD8 TCR clonotype expansion relates to phenotype and functional state associated with immunotherapy C_LIO_LINeoAg vaccines induce partially distinct macrophage remodeling from ICT C_LIO_LINeoAg vaccines synergize with ICT, exceeding combination CTLA-4/PD-1 ICT efficacy C_LI

immunology↗

The p38MAPK-MK2-HSP27 Pathway Regulates the mRNA Stability of the Senescence-Associated Secretory Phenotype

Age is a significant risk factor for the development of cancer. Both age-dependent accumulation of cell autonomous mutations within preneoplastic cells and increases in senescent stromal cells within the tumor microenvironment are thought to collaborate to drive tumorigenesis. Senescent cells express pro-tumorigenic factors termed the senescence-associated secretory phenotype (SASP), subject to a variety of regulatory mechanisms that are not fully elucidated. Previous work demonstrated that p38 mitogen-activated protein kinase (p38MAPK)-dependent regulation of AUF1 occupancy on SASP factor mRNAs post-transcriptionally stabilizes many SASP mRNAs and contributes to their increased expression. Here, we address the mechanism by which p38MAPK regulates AUF1s occupancy and activity on SASP factor mRNAs. We found that the p38MAPK-MK2-HSP27 pathway regulates both mRNA stability and AUF1 occupancy in cells induced to senesce. Furthermore, the tumor-promoting abilities of senescent stromal cells were lost upon inhibition of MK2, suggesting that this pathway is a viable therapeutic target within the tumor microenvironment.

cancer biology↗