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Dr. Amy Gillgrass
Department of Medicine, McMaster Immunology Research Centre (MIRC), Institute for Infectious Disease Research (IIDR), McMaster University, Hamilton, Canada

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0 HIV
0 Immunology
0 TB
0 Vaccines
0 infectious disease

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Immunology
Published: 05 March 2021 in Frontiers in Immunology
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Although antiretroviral therapy has transformed human immunodeficiency virus-type 1 (HIV-1) from a deadly infection into a chronic disease, it does not clear the viral reservoir, leaving HIV-1 as an uncurable infection. Currently, 1.2 million new HIV-1 infections occur globally each year, with little decrease over many years. Therefore, additional research is required to advance the current state of HIV management, find potential therapeutic strategies, and further understand the mechanisms of HIV pathogenesis and prevention strategies. Non-human primates (NHP) have been used extensively in HIV research and have provided critical advances within the field, but there are several issues that limit their use. Humanized mouse (Hu-mouse) models, or immunodeficient mice engrafted with human immune cells and/or tissues, provide a cost-effective and practical approach to create models for HIV research. Hu-mice closely parallel multiple aspects of human HIV infection and disease progression. Here, we highlight how innovations in Hu-mouse models have advanced HIV-1 research in the past decade. We discuss the effect of different background strains of mice, of modifications on the reconstitution of the immune cells, and the pros and cons of different human cells and/or tissue engraftment methods, on the ability to examine HIV-1 infection and immune response. Finally, we consider the newest advances in the Hu-mouse models and their potential to advance research in emerging areas of mucosal infections, understand the role of microbiota and the complex issues in HIV-TB co-infection. These innovations in Hu-mouse models hold the potential to significantly enhance mechanistic research to develop novel strategies for HIV prevention and therapeutics.

ACS Style

Amy Gillgrass; Jocelyn M. Wessels; Jack X. Yang; Charu Kaushic. Advances in Humanized Mouse Models to Improve Understanding of HIV-1 Pathogenesis and Immune Responses. Frontiers in Immunology 2021, 11, 1 .

AMA Style

Amy Gillgrass, Jocelyn M. Wessels, Jack X. Yang, Charu Kaushic. Advances in Humanized Mouse Models to Improve Understanding of HIV-1 Pathogenesis and Immune Responses. Frontiers in Immunology. 2021; 11 ():1.

Chicago/Turabian Style

Amy Gillgrass; Jocelyn M. Wessels; Jack X. Yang; Charu Kaushic. 2021. "Advances in Humanized Mouse Models to Improve Understanding of HIV-1 Pathogenesis and Immune Responses." Frontiers in Immunology 11, no. : 1.

Journal article
Published: 01 July 2017 in Breast Cancer Research
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Natural killer (NK) cells play a critical role in cancer immunosurveillance. Recent developments in NK cell ex-vivo expansion makes it possible to generate millions of activated NK cells from a small volume of peripheral blood. We tested the functionality of ex vivo expanded NK cells in vitro against breast cancer cell lines and in vivo using a xenograft mouse model. The study aim was to assess functionality and phenotype of expanded NK cells from breast cancer patients against breast cancer cell lines and autologous primary tumours. We used a well-established NK cell co-culture system to expand NK cells ex vivo from healthy donors and breast cancer patients and examined their surface marker expression. Moreover, we tested the ability of expanded NK cells to lyse the triple negative breast cancer and HER2-positive breast cancer cell lines MDA-MB-231 and MDA-MB-453, respectively. We also tested their ability to prevent tumour growth in vivo using a xenograft mouse model. Finally, we tested the cytotoxicity of expanded NK cells against autologous and allogeneic primary breast cancer tumours in vitro. After 3 weeks of culture we observed over 1000-fold expansion of NK cells isolated from either breast cancer patients or healthy donors. We also showed that the phenotype of expanded NK cells is comparable between those from healthy donors and cancer patients. Moreover, our results confirm the ability of ex vivo expanded NK cells to lyse tumour cell lines in vitro. While the cell lines examined had differential sensitivity to NK cell killing we found this was correlated with level of major histocompatibility complex (MHC) class I expression. In our in vivo model, NK cells prevented tumour establishment and growth in immunocompromised mice. Finally, we showed that NK cells expanded from the peripheral blood of breast cancer patients show high cytotoxicity against allogeneic and autologous patient-derived tumour cells in vitro. NK cells from breast cancer patients can be expanded similarly to those from healthy donors, have a high cytotoxic ability against breast cancer cell lines and patient-derived tumour cells, and can be compatible with current cancer treatments to restore NK cell function in cancer patients.

ACS Style

Mira M. Shenouda; Amy Gillgrass; Tina Nham; Richard Hogg; Amanda J. Lee; Marianne V. Chew; Mahsa Shafaei; Craig Aarts; Dean A. Lee; John Hassell; Anita Bane; Sukhbinder Dhesy-Thind; Ali A. Ashkar. Ex vivo expanded natural killer cells from breast cancer patients and healthy donors are highly cytotoxic against breast cancer cell lines and patient-derived tumours. Breast Cancer Research 2017, 19, 1 -14.

AMA Style

Mira M. Shenouda, Amy Gillgrass, Tina Nham, Richard Hogg, Amanda J. Lee, Marianne V. Chew, Mahsa Shafaei, Craig Aarts, Dean A. Lee, John Hassell, Anita Bane, Sukhbinder Dhesy-Thind, Ali A. Ashkar. Ex vivo expanded natural killer cells from breast cancer patients and healthy donors are highly cytotoxic against breast cancer cell lines and patient-derived tumours. Breast Cancer Research. 2017; 19 (1):1-14.

Chicago/Turabian Style

Mira M. Shenouda; Amy Gillgrass; Tina Nham; Richard Hogg; Amanda J. Lee; Marianne V. Chew; Mahsa Shafaei; Craig Aarts; Dean A. Lee; John Hassell; Anita Bane; Sukhbinder Dhesy-Thind; Ali A. Ashkar. 2017. "Ex vivo expanded natural killer cells from breast cancer patients and healthy donors are highly cytotoxic against breast cancer cell lines and patient-derived tumours." Breast Cancer Research 19, no. 1: 1-14.

Journal article
Published: 28 July 2016 in BMC Cancer
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Lymph node (LN) status is the most important prognostic variable used to guide ER positive (+) breast cancer treatment. While a positive nodal status is traditionally associated with a poor prognosis, a subset of these patients respond well to treatment and achieve long-term survival. Several gene signatures have been established as a means of predicting outcome of breast cancer patients, but the development and indication for use of these assays varies. Here we compare the capacity of two approved gene signatures and a third novel signature to predict outcome in distinct LN negative (-) and LN+ populations. We also examine biological differences between tumours associated with LN- and LN+ disease. Gene expression data from publically available data sets was used to compare the ability of Oncotype DX and Prosigna to predict Distant Metastasis Free Survival (DMFS) using an in silico platform. A novel gene signature (Ellen) was developed by including patients with both LN- and LN+ disease and using Prediction Analysis of Microarrays (PAM) software. Gene Set Enrichment Analysis (GSEA) was used to determine biological pathways associated with patient outcome in both LN- and LN+ tumors. The Oncotype DX gene signature, which only used LN- patients during development, significantly predicted outcome in LN- patients, but not LN+ patients. The Prosigna gene signature, which included both LN- and LN+ patients during development, predicted outcome in both LN- and LN+ patient groups. Ellen was also able to predict outcome in both LN- and LN+ patient groups. GSEA suggested that epigenetic modification may be related to poor outcome in LN- disease, whereas immune response may be related to good outcome in LN+ disease. We demonstrate the importance of incorporating lymph node status during the development of prognostic gene signatures. Ellen may be a useful tool to predict outcome of patients regardless of lymph node status, or for those with unknown lymph node status. Finally we present candidate biological processes, unique to LN- and LN+ disease, that may indicate risk of relapse.

ACS Style

Jessica G. Cockburn; Robin M. Hallett; Amy E. Gillgrass; Kay N. Dias; T. Whelan; M. N. Levine; John A. Hassell; Anita Bane. The effects of lymph node status on predicting outcome in ER+ /HER2- tamoxifen treated breast cancer patients using gene signatures. BMC Cancer 2016, 16, 555 .

AMA Style

Jessica G. Cockburn, Robin M. Hallett, Amy E. Gillgrass, Kay N. Dias, T. Whelan, M. N. Levine, John A. Hassell, Anita Bane. The effects of lymph node status on predicting outcome in ER+ /HER2- tamoxifen treated breast cancer patients using gene signatures. BMC Cancer. 2016; 16 (1):555.

Chicago/Turabian Style

Jessica G. Cockburn; Robin M. Hallett; Amy E. Gillgrass; Kay N. Dias; T. Whelan; M. N. Levine; John A. Hassell; Anita Bane. 2016. "The effects of lymph node status on predicting outcome in ER+ /HER2- tamoxifen treated breast cancer patients using gene signatures." BMC Cancer 16, no. 1: 555.

Journal article
Published: 16 April 2015 in BMC Cancer
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Natural Killer (NK) cells play an important role in tumor prevention, but once tumors form, the numbers as well as the cytotoxic functions of NK cells are reduced. IL-15 is a cytokine that increases and activates NK cells. Here we will examine the anti-tumor role of IL-15 in a spontaneous breast cancer model. To achieve this, Polyoma Middle T (MT) mice that form spontaneous breast cancer were crossed with mice that either overexpress IL-15 (IL-15 transgenic (TG)) or mice that lack IL-15 (IL-15 knockout (KO)). We compared survival curves and tumor formation in IL-15 KO/MT, MT and IL-15 TG/MT groups. In addition, the phenotype, activation and contribution of NK cells and CD8 T cells to tumor formation were examined in each of these mouse strains via flow cytometry, ELISA, adoptive transfer and antibody depletion experiments. IL-15KO/MT tumors formed and progressed to endpoint more quickly than MT tumors. These tumors displayed little apoptosis and poor CD8 T cell infiltration. In contrast, IL-15 TG/MT mice had increased survival and the tumors displayed extensive cell death, high proportions of activated NK cells and a higher infiltration of CD8 T cells than MT tumors. CD8 T cells in IL-15 TG/MT tumors were capable of secreting IFNγ, possessed markers of memory, did not display an exhausted phenotype and were frequently NK1.1+. Long-term antibody depletion studies in IL-15 TG/MT mice revealed that NK1.1+, but not CD8 T cells, were critical for tumor destruction. Lastly, human NK cells, when exposed to a similar cytokine environment as that found in IL-15TG/MT tumors, were capable of killing human breast cancer cells. This study reveals that high levels of IL-15 can promote tumor destruction and reduce metastasis in breast cancer via effects on NK1.1+ cells. Our results suggest that strategies aimed at increasing NK cell activation may be effective against solid epithelial cancers.

ACS Style

Amy E Gillgrass; Marianne V Chew; Tamara Krneta; Ali A Ashkar. Overexpression of IL-15 promotes tumor destruction via NK1.1+ cells in a spontaneous breast cancer model. BMC Cancer 2015, 15, 1 -15.

AMA Style

Amy E Gillgrass, Marianne V Chew, Tamara Krneta, Ali A Ashkar. Overexpression of IL-15 promotes tumor destruction via NK1.1+ cells in a spontaneous breast cancer model. BMC Cancer. 2015; 15 (1):1-15.

Chicago/Turabian Style

Amy E Gillgrass; Marianne V Chew; Tamara Krneta; Ali A Ashkar. 2015. "Overexpression of IL-15 promotes tumor destruction via NK1.1+ cells in a spontaneous breast cancer model." BMC Cancer 15, no. 1: 1-15.