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Article: PI3K Isoform Immunotherapy for Solid Tumours.

Scott, Jake / Rees, Lauren / Gallimore, Awen / Lauder, Sarah N

Current topics in microbiology and immunology

2022 Volume 436, Page(s) 369–392

Abstract: Improving the anti-tumour T cell response as a consequence of immunotherapy can result in eradication of tumour burden, however, the majority of patients fail with current treatment regimens and so novel immunotherapies with greater efficacy and improved ...

Abstract	Improving the anti-tumour T cell response as a consequence of immunotherapy can result in eradication of tumour burden, however, the majority of patients fail with current treatment regimens and so novel immunotherapies with greater efficacy and improved tolerability are needed. The phosphoinositide-3-kinase (PI3K) family members that are directly involved in cell signalling comprise PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ, with the latter two isoforms expressed primarily by leukocytes. The survival and optimal function of regulatory T cells (Treg) and myeloid-derived suppressor cells (MDSCs) is dependent on PI3Kδ, whereas tumour-associated macrophages (TAMs), use PI3Kγ. Blocking these signalling isoforms can boost development of effective anti-cancer immune responses and result in control of tumour burden. The dependence on different PI3K isoforms in immune cells makes targeting this pathway an attractive approach for tumour immunotherapy. Herein, we discuss how inhibiting specific PI3K isoforms in pro-tumoural Tregs, MDSCS and TAMs can unleash a powerful anti-tumour immune response, driven by CD8
MeSH term(s)	CD8-Positive T-Lymphocytes ; Humans ; Immune Checkpoint Inhibitors ; Immunotherapy ; Neoplasms/drug therapy ; Phosphatidylinositol 3-Kinase ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositols/therapeutic use ; Phosphoinositide-3 Kinase Inhibitors ; Protein Isoforms/genetics ; Protein Isoforms/therapeutic use
Chemical Substances	Immune Checkpoint Inhibitors ; Phosphatidylinositols ; Phosphoinositide-3 Kinase Inhibitors ; Protein Isoforms ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
Language	English
Publishing date	2022-09-29
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	210099-X
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-031-06566-8_16
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Article ; Online: Sequential targeting of PI3Kδ and LAG3 as an effective anti-cancer approach.

Lauder, Sarah N / Vanhaesebroeck, Bart / Gallimore, Awen

British journal of cancer

2021 Volume 125, Issue 4, Page(s) 467–469

Abstract: Emerging studies have demonstrated the potential of PI3Kδ blockade as an immunotherapy for solid tumours. In pre-clinical models, we recently demonstrated that anti-LAG3 immune checkpoint blockade vastly potentiated PI3Kδ-based immunotherapy, enabling ... ...

Abstract	Emerging studies have demonstrated the potential of PI3Kδ blockade as an immunotherapy for solid tumours. In pre-clinical models, we recently demonstrated that anti-LAG3 immune checkpoint blockade vastly potentiated PI3Kδ-based immunotherapy, enabling successful tumour control in all treated mice.
MeSH term(s)	Animals ; Antigens, CD/immunology ; Class I Phosphatidylinositol 3-Kinases/immunology ; Drug Resistance, Neoplasm/drug effects ; Drug Synergism ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Immunotherapy ; Mice ; Neoplasms/drug therapy ; Neoplasms/immunology ; Tumor Microenvironment ; Xenograft Model Antitumor Assays ; Lymphocyte Activation Gene 3 Protein
Chemical Substances	Antigens, CD ; Immune Checkpoint Inhibitors ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CD protein, human (EC 2.7.1.137) ; Lymphocyte Activation Gene 3 Protein
Language	English
Publishing date	2021-04-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-021-01285-1
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Article ; Online: Treg-driven tumour control by PI3Kδ inhibition limits myeloid-derived suppressor cell expansion.

Lauder, Sarah N / Smart, Kathryn / Bart, Valentina M T / Pires, Ana / Scott, Jake / Milutinovic, Stefan / Godkin, Andrew / Vanhaesebroeck, Bart / Gallimore, Awen

British journal of cancer

2022 Volume 127, Issue 9, Page(s) 1595–1602

Abstract: Background: Recent studies have demonstrated that blocking the PI3Kδ signalling enzyme (by administering a small molecule inhibitor, PI-3065) can potently improve the anti-tumour T-cell response through direct inhibition of Tregs. This treatment also ... ...

Abstract	Background: Recent studies have demonstrated that blocking the PI3Kδ signalling enzyme (by administering a small molecule inhibitor, PI-3065) can potently improve the anti-tumour T-cell response through direct inhibition of Tregs. This treatment also has a negative impact on MDSC numbers but the primary mechanism driving this effect has remained unclear. Methods: The 4T1 breast cancer mouse model was used in combination with PI-3065 to gain insights into the effect of PI3Kδ inhibition on MDSCs. Results: PI-3065 treatment resulted in a concomitant reduction in MDSC expansion and tumour size. However, targeting Tregs independent of PI-3065 was also associated with reduced tumour volume and MDSC numbers. Surgical removal of tumours resulted in a rapid and significant decline in MDSC numbers, whilst ex vivo studies using cells from PI-3065-treated mice demonstrated no direct effect of the inhibitor on MDSC activity. Conclusions: Our data suggest that MDSCs are not inhibited directly by PI-3065 treatment but that their reduced recruitment and immunosuppression within the tumour microenvironment is an indirect consequence of PI3Kδ-inhibition-driven tumour control. This indicates that PI3Kδ inhibition drives tumour immunity by breaking down multiple immunosuppressive pathways through both direct mechanisms (on Treg) and indirect mechanisms, secondary to tumour control (on MDSCs).
MeSH term(s)	Animals ; Mice ; Myeloid-Derived Suppressor Cells ; T-Lymphocytes, Regulatory ; Neoplasms ; Tumor Microenvironment ; Cell Proliferation
Language	English
Publishing date	2022-08-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-022-01917-0
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Article ; Online: Three-dimensional Imaging Reveals Immune-driven Tumor-associated High Endothelial Venules as a Key Correlate of Tumor Rejection Following Depletion of Regulatory T Cells.

Milutinovic, Stefan / Abe, Jun / Jones, Emma / Kelch, Inken / Smart, Kathryn / Lauder, Sarah N / Somerville, Michelle / Ware, Carl / Godkin, Andrew / Stein, Jens V / Bogle, Gib / Gallimore, Awen

Cancer research communications

2023 Volume 2, Issue 12, Page(s) 1641–1656

Abstract: High endothelial venules (HEV) are specialized post capillary venules that recruit naïve T cells and B cells into secondary lymphoid organs (SLO) such as lymph nodes (LN). Expansion of HEV networks in SLOs occurs following immune activation to support ... ...

Abstract	High endothelial venules (HEV) are specialized post capillary venules that recruit naïve T cells and B cells into secondary lymphoid organs (SLO) such as lymph nodes (LN). Expansion of HEV networks in SLOs occurs following immune activation to support development of an effective immune response. In this study, we used a carcinogen-induced model of fibrosarcoma to examine HEV remodeling after depletion of regulatory T cells (Treg). We used light sheet fluorescence microscopy imaging to visualize entire HEV networks, subsequently applying computational tools to enable topological mapping and extraction of numerical descriptors of the networks. While these analyses revealed profound cancer- and immune-driven alterations to HEV networks within LNs, these changes did not identify successful responses to treatment. The presence of HEV networks within tumors did however clearly distinguish responders from nonresponders. Finally, we show that a successful treatment response is dependent on coupling tumor-associated HEV (TA-HEV) development to T-cell activation implying that T-cell activation acts as the trigger for development of TA-HEVs which subsequently serve to amplify the immune response by facilitating extravasation of T cells into the tumor mass.
MeSH term(s)	Humans ; T-Lymphocytes, Regulatory ; Venules ; Imaging, Three-Dimensional ; Neoplasms ; Lymph Nodes
Language	English
Publishing date	2023-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-21-0123
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Article ; Online: Magnitude of venous or capillary blood-derived SARS-CoV-2-specific T cell response determines COVID-19 immunity.

Scurr, Martin J / Lippiatt, George / Capitani, Lorenzo / Bentley, Kirsten / Lauder, Sarah N / Smart, Kathryn / Somerville, Michelle S / Rees, Tara / Stanton, Richard J / Gallimore, Awen / Hindley, James P / Godkin, Andrew

Nature communications

2022 Volume 13, Issue 1, Page(s) 5422

Abstract: T cells specific for SARS-CoV-2 are thought to protect against infection and development of COVID-19, but direct evidence for this is lacking. Here, we associated whole-blood-based measurement of SARS-CoV-2-specific interferon-γ-positive T cell responses ...

Abstract	T cells specific for SARS-CoV-2 are thought to protect against infection and development of COVID-19, but direct evidence for this is lacking. Here, we associated whole-blood-based measurement of SARS-CoV-2-specific interferon-γ-positive T cell responses with positive COVID-19 diagnostic (PCR and/or lateral flow) test results up to 6 months post-blood sampling. Amongst 148 participants donating venous blood samples, SARS-CoV-2-specific T cell response magnitude is significantly greater in those who remain protected versus those who become infected (P < 0.0001); relatively low magnitude T cell response results in a 43.2% risk of infection, whereas high magnitude reduces this risk to 5.4%. These findings are recapitulated in a further 299 participants testing a scalable capillary blood-based assay that could facilitate the acquisition of population-scale T cell immunity data (14.9% and 4.4%, respectively). Hence, measurement of SARS-CoV-2-specific T cells can prognosticate infection risk and should be assessed when monitoring individual and population immunity status.
MeSH term(s)	Antibodies, Viral ; COVID-19 ; Humans ; Interferon-gamma ; Polymerase Chain Reaction ; SARS-CoV-2 ; T-Lymphocytes
Chemical Substances	Antibodies, Viral ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2022-09-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32985-8
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Article ; Online: Acquisition of suppressive function by conventional T cells limits antitumor immunity upon T

Science immunology

2023 Volume 8, Issue 90, Page(s) eabo5558

Abstract: Regulatory T ( ... ...

Abstract	Regulatory T (T
MeSH term(s)	Mice ; Humans ; Animals ; T-Lymphocytes, Regulatory ; Interleukin-10/metabolism ; Neoplasms/therapy ; Neoplasms/metabolism ; Immunotherapy ; Forkhead Transcription Factors/metabolism
Chemical Substances	Interleukin-10 (130068-27-8) ; Forkhead Transcription Factors
Language	English
Publishing date	2023-12-15
Publishing country	United States
Document type	Journal Article
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.abo5558
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Article ; Online: Primary breast tumours but not lung metastases induce protective anti-tumour immune responses after Treg-depletion.

Hughes, Ellyn / Lauder, Sarah N / Smart, Kathryn / Bloom, Anja / Scott, Jake / Jones, Emma / Somerville, Michelle / Browne, Molly / Blainey, Andrew / Godkin, Andrew / Ager, Ann / Gallimore, Awen

Cancer immunology, immunotherapy : CII

2020 Volume 69, Issue 10, Page(s) 2063–2073

Abstract: Although metastatic disease is responsible for the majority of cancer deaths, tests of novel immunotherapies in mouse tumour models often focus on primary tumours without determining whether these therapies also target metastatic disease. This study ... ...

Abstract	Although metastatic disease is responsible for the majority of cancer deaths, tests of novel immunotherapies in mouse tumour models often focus on primary tumours without determining whether these therapies also target metastatic disease. This study examined the impact of depleting Foxp3
MeSH term(s)	Animals ; Female ; Forkhead Transcription Factors/metabolism ; Immunotherapy/methods ; Lung Neoplasms/immunology ; Lung Neoplasms/secondary ; Lung Neoplasms/therapy ; Lymphocyte Depletion/methods ; Lymphocytes, Tumor-Infiltrating/drug effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Mice ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Triple Negative Breast Neoplasms/immunology ; Triple Negative Breast Neoplasms/pathology ; Triple Negative Breast Neoplasms/therapy
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse
Language	English
Publishing date	2020-05-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-020-02603-x
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Zs.A 1237: Show issues

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Article ; Online: The Ussing chamber system for measuring intestinal permeability in health and disease.

Thomson, Amanda / Smart, Kathryn / Somerville, Michelle S / Lauder, Sarah N / Appanna, Gautham / Horwood, James / Sunder Raj, Lawrence / Srivastava, Brijesh / Durai, Dharmaraj / Scurr, Martin J / Keita, Åsa V / Gallimore, Awen M / Godkin, Andrew

BMC gastroenterology

2019 Volume 19, Issue 1, Page(s) 98

Abstract: Background: The relationship between intestinal epithelial integrity and the development of intestinal disease is of increasing interest. A reduction in mucosal integrity has been associated with ulcerative colitis, Crohn's disease and potentially could ...

Abstract	Background: The relationship between intestinal epithelial integrity and the development of intestinal disease is of increasing interest. A reduction in mucosal integrity has been associated with ulcerative colitis, Crohn's disease and potentially could have links with colorectal cancer development. The Ussing chamber system can be utilised as a valuable tool for measuring gut integrity. Here we describe step-by-step methodology required to measure intestinal permeability of both mouse and human colonic tissue samples ex vivo, using the latest equipment and software. This system can be modified to accommodate other tissues. Methods: An Ussing chamber was constructed and adapted to support both mouse and human tissue to measure intestinal permeability, using paracellular flux and electrical measurements. Two mouse models of intestinal inflammation (dextran sodium sulphate treatment and T regulatory cell depletion using C57BL/6-FoxP3 Results: Distinct regional differences in permeability were consistently identified within mouse and healthy human colon. In particular, mice showed increased permeability in the mid colonic region. In humans the left colon is more permeable than the right. Furthermore, inflammatory conditions induced chemically or due to autoimmunity reduced intestinal integrity, validating the use of the system. Conclusions: The Ussing chamber has been used for many years to measure barrier function. However, a clear and informative methods paper describing the setup of modern equipment and step-by-step procedure to measure mouse and human intestinal permeability isn't available. The Ussing chamber system methodology we describe provides such detail to guide investigation of gut integrity.
MeSH term(s)	Animals ; Colitis/chemically induced ; Colitis/metabolism ; Colon/metabolism ; Dextran Sulfate ; Electrodiagnosis/instrumentation ; Electrodiagnosis/methods ; Fluorescence ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Mice, Inbred C57BL ; Permeability
Chemical Substances	Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2019-06-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041351-8
ISSN	1471-230X ; 1471-230X
ISSN (online)	1471-230X
ISSN	1471-230X
DOI	10.1186/s12876-019-1002-4
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Article ; Online: Immune Remodeling of the Extracellular Matrix Drives Loss of Cancer Stem Cells and Tumor Rejection.

Pires, Ana / Greenshields-Watson, Alexander / Jones, Emma / Smart, Kathryn / Lauder, Sarah N / Somerville, Michelle / Milutinovic, Stefan / Kendrick, Howard / Hindley, James P / French, Rhiannon / Smalley, Matthew J / Watkins, William J / Andrews, Robert / Godkin, Andrew / Gallimore, Awen

Cancer immunology research

2020 Volume 8, Issue 12, Page(s) 1520–1531

Abstract: The nature of the tumor microenvironment (TME) influences the ability of tumor-specific T cells to control tumor growth. In this study, we performed an unbiased comparison of the TME of regulatory T-cell (Treg)-replete and Treg-depleted carcinogen- ... ...

Abstract	The nature of the tumor microenvironment (TME) influences the ability of tumor-specific T cells to control tumor growth. In this study, we performed an unbiased comparison of the TME of regulatory T-cell (Treg)-replete and Treg-depleted carcinogen-induced tumors, including Treg-depleted responding (regressing) and non-responding (growing) tumors. This analysis revealed an inverse relationship between extracellular matrix (ECM) and T-cell infiltrates where responding tumors were T-cell rich and ECM poor, whereas the converse was observed in non-responder tumors. For this reason, we hypothesized that the ECM acted as a barrier to successful T-cell infiltration and tumor rejection. However, further experiments revealed that this was not the case but instead showed that an effective T-cell response dramatically altered the density of ECM in the TME. Along with loss of ECM and high numbers of infiltrating T cells, responder tumors were distinguished by the development of lymphatic and blood vessel networks with specialized immune function. ECM-rich tumors exhibited a stem cell-like gene expression profile and superior tumor-initiating capacity, whereas such features were absent in responder tumors. Overall, these findings define an extended role for an effective immune response, not just in direct killing of tumor cells but in widescale remodeling of the TME to favor loss of ECM, elimination of cancer stem cells, and propagation of adaptive immunity.
MeSH term(s)	Animals ; Cell Line, Tumor ; Extracellular Matrix ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Language	English
Publishing date	2020-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-20-0070
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Article ; Online: Antiviral therapy can reverse the development of immune senescence in elderly mice with latent cytomegalovirus infection.

Beswick, Mark / Pachnio, Annette / Lauder, Sarah N / Sweet, Clive / Moss, Paul A

Journal of virology

2012 Volume 87, Issue 2, Page(s) 779–789

Abstract: Cytomegalovirus (CMV) infection leads to the development of adaptive and humoral immune responses that are among the largest for any pathogen, and intriguingly, the magnitude of the immune response increases with age, a phenomenon termed "memory ... ...

Abstract	Cytomegalovirus (CMV) infection leads to the development of adaptive and humoral immune responses that are among the largest for any pathogen, and intriguingly, the magnitude of the immune response increases with age, a phenomenon termed "memory inflation." Elevated CMV-specific immunity has been correlated with an increased mortality rate in elderly individuals and with impaired vaccination responses. The latent phase of CMV infection is characterized by intermittent episodes of subclinical viral reactivation and the production of immunogenic transcripts that may maintain memory inflation of virus-specific cytotoxic lymphocytes. However, the relative importance of CMV reactivation in the development of memory inflation is uncertain, as is the potential for antiviral treatment to reverse this effect. Here, we administered valaciclovir for up to 12 months in mice with established murine CMV (MCMV) infection. Treatment reduced the magnitude of the MCMV-specific CD8(+) T-lymphocyte response by 80%, and the residual MCMV tetramer-specific lymphocytes exhibited a less differentiated phenotype. In addition, latent MCMV infection suppressed the proportion of naïve CD8(+) T cells by 60% compared to antiviral-treated mice or MCMV-negative animals. Furthermore, treatment led to a reduction in influenza A viral loads following a challenge in elderly MCMV-infected animals and also reduced the differentiation of influenza virus-specific cytotoxic lymphocytes. These observations demonstrate that MCMV-specific memory inflation is maintained by viral replication and that therapeutic intervention could lead to improved immune function.
MeSH term(s)	Acyclovir/administration & dosage ; Acyclovir/analogs & derivatives ; Animals ; Antiviral Agents/administration & dosage ; CD8-Positive T-Lymphocytes/immunology ; Cytomegalovirus Infections/drug therapy ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/veterinary ; Female ; Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Muromegalovirus/immunology ; Muromegalovirus/pathogenicity ; Valacyclovir ; Valine/administration & dosage ; Valine/analogs & derivatives ; Virus Activation ; Virus Latency
Chemical Substances	Antiviral Agents ; Valine (HG18B9YRS7) ; Valacyclovir (MZ1IW7Q79D) ; Acyclovir (X4HES1O11F)
Language	English
Publishing date	2012-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.02427-12
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