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Biology subjects

Munz, C.

Publications and source records attributed to Munz, C..

3 recordsLinked to original sources

Epstein Barr virus infection induces tissue-resident memory T cells in mucosal lymphoid tissues

Epstein Barr virus (EBV) contributes to around 2% of all tumors worldwide. Simultaneously, more than 90% of healthy human adults persistently carry EBV without clinical symptoms. In most EBV carriers it is thought that virus-induced tumorigenesis is prevented by cell-mediated immunity. Specifically, memory CD8+ T cells recognize EBV-infected cells during latent and lytic infection. Using a symptomatic primary infection model, similar to infectious mononucleosis (IM), we found EBV induced CD8+ tissue resident memory T cells (TRMs) in mice with a humanized immune system. These human TRMs were preferentially established after intranasal EBV infection in nasal-associated lymphoid tissues (NALT), equivalent to tonsils, the primary site of EBV infection in humans. They expressed canonical TRM markers, including CD69, CD103 and BLIMP-1, as well as Granzyme B, CD107a and CCL5, while demonstrating reduced CD27 expression and proliferation by Ki-67 expression. Despite cytotoxic activity and cytokine production ex vivo, these TRMs failed to control EBV viral loads in the NALT during infection although effector memory T cells (TEMs) controlled viral titers in spleen and blood. Overall, TRMs in mucosal lymphoid tissues are established by EBV infection, but primarily systemic CD8+ T cell expansion seems to attenuate viral loads in the context of IM-like infection. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/565960v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@1cc2a9borg.highwire.dtl.DTLVardef@1013ea1org.highwire.dtl.DTLVardef@b6be98org.highwire.dtl.DTLVardef@19af7c7_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Human effector CD8+ T cells with an exhausted-like phenotype control tumor growth in vivo

BackgroundHumanized tumor models could be particularly valuable for cancer immunotherapy research, as they may better reflect human-specific aspects of the interfaces between tumor and immune system of human cancer. However, endogenous antitumor immunity in humanized models is still largely undefined. MethodsWe established a novel autologous humanized mouse tumor model by using NSG mice reconstituted with human immune cells from hematopoietic progenitors and tumors generated from transformed autologous human B cells. We demonstrate growth of solid lymphoid tumors after subcutaneous implantation, infiltration by endogenous human immune cells and immunocompetence of the model. FindingsWe found human T cell subsets described in human cancer, including progenitor exhausted (Tpex), terminally exhausted (Tex-term) and tissue-resident (TRM) cells in tumor-bearing humanized mice with accumulation of Tex-term and TRM in the tumor. In addition, we identified tumor-reactive CD8+ T cells through expression of CD137. This subpopulation of de novo arising human CD137+ CD8+ T cells displayed a highly proliferative, fully activated effector and exhausted-like phenotype with enhanced expression of activation and exhaustion markers like PD-1, CD39, CD160, TIM-3, TIGIT and TOX, the senescence marker CD57 (B3GAT1) and cytolytic effector molecules such as PRF1, GZMH and NKG7. Moreover, these CD137+ CD8+ T cells exhibited tumor-specific clonal expansion and presented signature overlap with tumor-reactive CD8+ T cells described in human cancer. We demonstrate superior anticancer activity of this exhausted-like human CD8+ T cell subset by adoptive transfer experiments using recipients bearing autologous human tumors. Mice adoptively transferred with CD137+ CD8+ T cells showed reduced tumor growth and higher CD8+ T cell tumor infiltration, correlating with control of human tumors. InterpretationWe established an immunocompetent humanized tumor model, providing a tool for immunotherapy research and defined effective anticancer activity of human effector CD8+ T cells with an exhausted-like phenotype, supporting clinical exploration of such cells in adoptive T cell therapies. FundingSwiss Cancer Research foundation. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSAntitumor immune responses and outcome of immunotherapeutic interventions are not always consistent between mouse models of cancer and data available in humans. This may be due to species-specific differences, therefore models with a potential for better translatability are needed, such as humanized mouse models. However, there is limited data on human antitumor T cell immunity in humanized mice. Added value of this studyIn this study, we established an immunocompetent humanized tumor model that recapitulates hallmarks of human antitumor T cell responses, offering the possibility for further translational investigation of the interface between human tumors and endogenous anticancer immunity. Furthermore, using functional in vitro assays and adoptive transfer, our study demonstrates the key importance of human effector CD8+ T cells with an activated and exhausted-like phenotype in the antitumor immune response. Implications of all the available evidenceThe autologous humanized tumor model provided in this study can serve as a tool to elucidate human-specific immune features. By bridging a gap between syngeneic mouse tumor models and human-specific antitumor immune responses, the model may help open up avenues for greater translatability of preclinical data. Our findings suggest that exhausted-like effector CD8+ T cells can be harnessed for clinical development of adoptive T cell therapies.

immunology↗

Clearance of genome-damaged cells from the hematopoietic system via p53 without contribution by the cGAS/STING axis

Cell-intrinsic response patterns control risks arising from genome-damage, preventing malignant transformation. The DNA sensor cyclic-GMP-AMP synthase (cGAS) has emerged as a new principle detecting genome damage, as it can be triggered by aberrant self-DNA. Stimulator of interferon genes (STING)-activation downstream of cGAS can drive cells into senescence or cell death and induces antiproliferative type I interferon (IFN) and pro-apoptotic tumor necrosis factor responses. Herein, we investigated how DNA damage-driven activation of cGAS/STING signaling impacts on hematopoiesis. Defective ribonucleotide excision repair (RER) in the hematopoietic system caused chromosomal instability as well as robust activation of the cGAS/STING/IFN axis, and compromised hematopoietic stem cell function, resulting in cytopenia and ultimately leukemia. Whereas loss of p53 largely rescued RER-deficient hematopoiesis at the cost of further accelerated leukemogenesis, the additional inactivation of cGAS, STING or type I IFN signaling had no detectable effect on blood cell generation and leukemia development. Moreover, cGAS-deficient hematopoiesis showed unaltered responses to spontaneous or acute DNA damage. Our data demonstrate that the cGAS/STING pathway is dispensable for the hematopoietic system coping with chronic or acute DNA damage and does not protect against leukemic transformation in the absence of RER.

cell biology↗