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@ -2083,6 +2083,198 @@ CONCLUSIONS: We developed a simplified, semi-closed system for the initial selec
publisher = {Elsevier {BV}}, publisher = {Elsevier {BV}},
} }
@Article{Liu2019,
author = {Jie Liu and Guangyu Zhou and Li Zhang and Qi Zhao},
journal = {Frontiers in Immunology},
title = {Building Potent Chimeric Antigen Receptor T Cells With {CRISPR} Genome Editing},
year = {2019},
month = {mar},
volume = {10},
doi = {10.3389/fimmu.2019.00456},
publisher = {Frontiers Media {SA}},
}
@Article{Wiebking2020,
author = {Volker Wiebking and Ciaran M. Lee and Nathalie Mostrel and Premanjali Lahiri and Rasmus Bak and Gang Bao and Maria Grazia Roncarolo and Alice Bertaina and Matthew H. Porteus},
journal = {Haematologica},
title = {Genome editing of donor-derived T-cells to generate allogenic chimeric antigen receptor-modified T cells: Optimizing $\upalpha$$\upbeta$ T cell-depleted haploidentical hematopoietic stem cell transplantation},
year = {2020},
month = {apr},
number = {3},
pages = {847--858},
volume = {106},
doi = {10.3324/haematol.2019.233882},
publisher = {Ferrata Storti Foundation (Haematologica)},
}
@Article{Provasi2012,
author = {Elena Provasi and Pietro Genovese and Angelo Lombardo and Zulma Magnani and Pei-Qi Liu and Andreas Reik and Victoria Chu and David E Paschon and Lei Zhang and Jurgen Kuball and Barbara Camisa and Attilio Bondanza and Giulia Casorati and Maurilio Ponzoni and Fabio Ciceri and Claudio Bordignon and Philip D Greenberg and Michael C Holmes and Philip D Gregory and Luigi Naldini and Chiara Bonini},
journal = {Nature Medicine},
title = {Editing T cell specificity towards leukemia by zinc finger nucleases and lentiviral gene transfer},
year = {2012},
month = {apr},
number = {5},
pages = {807--815},
volume = {18},
doi = {10.1038/nm.2700},
publisher = {Springer Science and Business Media {LLC}},
}
@Article{Berdien2014,
author = {B Berdien and U Mock and D Atanackovic and B Fehse},
journal = {Gene Therapy},
title = {{TALEN}-mediated editing of endogenous T-cell receptors facilitates efficient reprogramming of T lymphocytes by lentiviral gene transfer},
year = {2014},
month = {mar},
number = {6},
pages = {539--548},
volume = {21},
doi = {10.1038/gt.2014.26},
publisher = {Springer Science and Business Media {LLC}},
}
@Article{Themeli2015,
author = {Maria Themeli and Isabelle Rivi{\`{e}}re and Michel Sadelain},
journal = {Cell Stem Cell},
title = {New Cell Sources for T Cell Engineering and Adoptive Immunotherapy},
year = {2015},
month = {apr},
number = {4},
pages = {357--366},
volume = {16},
doi = {10.1016/j.stem.2015.03.011},
publisher = {Elsevier {BV}},
}
@Article{Decker2012,
author = {Thomas Decker and Gerhard Fischer and Wolfgang Bücke and Philipp Bücke and Frank Stotz and Andreas Grüneberger and Martina Gropp-Meier and Günther Wiedemann and Christine Pfeiffer and Christian Peschel and Katharina Götze},
journal = {Journal of Cancer Research and Clinical Oncology},
title = {Increased number of regulatory T cells (T-regs) in the peripheral blood of patients with Her-2/neu-positive early breast cancer},
year = {2012},
month = {jul},
number = {11},
pages = {1945--1950},
volume = {138},
doi = {10.1007/s00432-012-1258-3},
publisher = {Springer Science and Business Media {LLC}},
}
@Article{Goldstein2012,
author = {Matthew J. Goldstein and Holbrook E. Kohrt and Roch Houot and Bindu Varghese and Jack T. Lin and Erica Swanson and Ronald Levy},
journal = {Cancer Research},
title = {Adoptive Cell Therapy for Lymphoma with {CD}4 T Cells Depleted of {CD}137-Expressing Regulatory T Cells},
year = {2012},
month = {jan},
number = {5},
pages = {1239--1247},
volume = {72},
doi = {10.1158/0008-5472.can-11-3375},
publisher = {American Association for Cancer Research ({AACR})},
}
@Article{Drela2004,
author = {Nadzieja Drela and Ahmad Jalili and Rafal Kaminski and Katarzyna Kozar and Marek Jak<61>bisiak and Witold Lasek and Grzegorz Basak and Tomasz Switaj and Anna B. Jakubowska and Piotr J. Wysocki and Andrzej Mackiewicz},
journal = {Cancer Immunology, Immunotherapy},
title = {Complete tumour regressions induced by vaccination with {IL}-12 gene-transduced tumour cells in combination with {IL}-15 in a melanoma model in mice},
year = {2004},
month = {apr},
number = {4},
pages = {363--372},
volume = {53},
doi = {10.1007/s00262-003-0449-9},
publisher = {Springer Science and Business Media {LLC}},
}
@Article{Rankin2003,
author = {Rankin, Erinn B. and Yu, Duonan and Jiang, Jiu and Shen, Hao and Pearce, Edward J. and Goldschmidt, Michael H. and Levy, David E. and Golovkina, Tatyana V. and Hunter, Christopher A. and Thomas-Tikhonenko, Andrei},
journal = {Cancer biology and therapy},
title = {An essential role of {Th1} responses and interferon gamma in infection-mediated suppression of neoplastic growth.},
year = {2003},
issn = {1538-4047},
pages = {687--693},
volume = {2},
abstract = {We had previously demonstrated that in mice acute toxoplasmosis leads to systemic inhibition of angiogenesis and, consequently, strong suppression of neoplastic growth. Here we investigated the role of Th1 cytokines, in particular interferon gamma (IFN-gamma), in this phenomenon. Besides toxoplasma, neoplastic growth was readily blocked during acute infection with other Th1 response-inducing pathogens such as Listeria monocytogenes and lymphocytic choriomeningitis virus (LCMV). In contrast, chronic infection with LCMV (when Th1 responses were strongly suppressed) and acute infection with Schistosoma mansoni (when Th2 responses predominated) afforded no anti-tumor protection. To corroborate the involvement of Th1 cytokines in infection-mediated suppression of neoplastic growth, we utilized mice deficient in interleukin-10 (IL10), a suppressor of Th1 responses. When challenged with B16 cells concomitantly with toxoplasma infection, both IL10-null and wild type mice exhibited resistance to neoplastic growth. However, tumors borne by IL10-null animals were even smaller than those borne by their wild type counterparts. This enhanced resistance correlated with dramatically elevated levels of circulating IFN-gamma, a principal Th1 cytokine. Furthermore, while interleukin-12 and tumor necrosis factor a were dispensable for tumor suppression, in animals deficient in IFN-gamma production or signaling, tumor growth and neovascularization were markedly enhanced. Interestingly, the enhancement was also apparent in uninfected animals suggesting that IFN-gamma and its anti-angiogenic effects underlie both infection-dependent and -independent tumor surveillance.},
chemicals = {Culture Media, Conditioned, Cytokines, Drug Combinations, Laminin, Proteoglycans, Vascular Endothelial Growth Factor A, matrigel, Interleukin-10, Interferon-gamma, Collagen},
citation-subset = {IM},
completed = {2004-09-13},
country = {United States},
issn-linking = {1538-4047},
issue = {6},
keywords = {Acute Disease; Animals; Cell Line, Tumor; Cell Transplantation; Clone Cells; Collagen, metabolism; Culture Media, Conditioned, analysis; Cytokines, immunology; Drug Combinations; Infections, blood, immunology; Interferon-gamma, analysis, immunology; Interleukin-10, deficiency; Laminin, metabolism; Listeria monocytogenes, pathogenicity; Lymphocytic choriomeningitis virus, pathogenicity; Melanoma, Experimental, blood, immunology, pathology; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Biological; Neovascularization, Pathologic; Proteoglycans, metabolism; Th1 Cells, immunology; Time Factors; Toxoplasma, pathogenicity; Toxoplasmosis; Vascular Endothelial Growth Factor A, analysis, genetics, metabolism},
nlm-id = {101137842},
owner = {NLM},
pii = {557},
pmid = {14688478},
pubmodel = {Print},
pubstate = {ppublish},
revised = {2020-09-30},
}
@Article{Luheshi2013,
author = {Nadia Luheshi and Gareth Davies and Edmund Poon and Kimberley Wiggins and Matthew McCourt and James Legg},
journal = {European Journal of Immunology},
title = {Th1 cytokines are more effective than Th2 cytokines at licensing anti-tumour functions in {CD}40-activated human macrophages in vitro},
year = {2013},
month = {oct},
number = {1},
pages = {162--172},
volume = {44},
doi = {10.1002/eji.201343351},
publisher = {Wiley},
}
@Article{Grotz2015,
author = {Travis E Grotz and James W Jakub and Aaron S Mansfield and Rachel Goldenstein and Elizabeth Ann L Enninga and Wendy K Nevala and Alexey A Leontovich and Svetomir N Markovic},
journal = {{OncoImmunology}},
title = {Evidence of Th2 polarization of the sentinel lymph node ({SLN}) in melanoma},
year = {2015},
month = {jun},
number = {8},
pages = {e1026504},
volume = {4},
doi = {10.1080/2162402x.2015.1026504},
publisher = {Informa {UK} Limited},
}
@Article{Ando2019,
author = {Makoto Ando and Minako Ito and Tanakorn Srirat and Taisuke Kondo and Akihiko Yoshimura},
journal = {Immunological Medicine},
title = {Memory T cell, exhaustion, and tumor immunity},
year = {2019},
month = {dec},
number = {1},
pages = {1--9},
volume = {43},
doi = {10.1080/25785826.2019.1698261},
publisher = {Informa {UK} Limited},
}
@Article{Wherry2015,
author = {E. John Wherry and Makoto Kurachi},
journal = {Nature Reviews Immunology},
title = {Molecular and cellular insights into T cell exhaustion},
year = {2015},
month = {jul},
number = {8},
pages = {486--499},
volume = {15},
doi = {10.1038/nri3862},
publisher = {Springer Science and Business Media {LLC}},
}
@Article{Zheng2017,
author = {Chunhong Zheng and Liangtao Zheng and Jae-Kwang Yoo and Huahu Guo and Yuanyuan Zhang and Xinyi Guo and Boxi Kang and Ruozhen Hu and Julie Y. Huang and Qiming Zhang and Zhouzerui Liu and Minghui Dong and Xueda Hu and Wenjun Ouyang and Jirun Peng and Zemin Zhang},
journal = {Cell},
title = {Landscape of Infiltrating T Cells in Liver Cancer Revealed by Single-Cell Sequencing},
year = {2017},
month = {jun},
number = {7},
pages = {1342--1356.e16},
volume = {169},
doi = {10.1016/j.cell.2017.05.035},
publisher = {Elsevier {BV}},
}
@Comment{jabref-meta: databaseType:bibtex;} @Comment{jabref-meta: databaseType:bibtex;}
@Comment{jabref-meta: grouping: @Comment{jabref-meta: grouping:

49
tex/thesis.tex
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@ -152,6 +152,9 @@
\newacronym{mse}{MSE}{mean squared error} \newacronym{mse}{MSE}{mean squared error}
\newacronym{loocv}{LOO-CV}{leave-one-out cross validation} \newacronym{loocv}{LOO-CV}{leave-one-out cross validation}
\newacronym{hsqc}{HSQC}{heteronuclear single quantum coherence} \newacronym{hsqc}{HSQC}{heteronuclear single quantum coherence}
\newacronym{hla}{HLA}{human leukocyte antigen}
\newacronym{zfn}{ZFN}{zinc-finger nuclease}
\newacronym{talen}{TALEN}{transcription activator-like effector nuclease}
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%% %%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
% SI units for uber nerds % SI units for uber nerds
@ -574,8 +577,6 @@ present our final conclusions in Chapter~\ref{conclusions}.
\subsection{microcarriers in bioprocessing} \subsection{microcarriers in bioprocessing}
% https://www.sciencedirect.com/science/article/pii/S0928493118338001#bb0010
Microcarriers have historically been used to grow a number of adherent cell Microcarriers have historically been used to grow a number of adherent cell
types for a variety of applications. They were introduced in 1967 as a means to types for a variety of applications. They were introduced in 1967 as a means to
grow adherent cells `in suspension', effectively turning a 2D flask system into grow adherent cells `in suspension', effectively turning a 2D flask system into
@ -632,8 +633,6 @@ the use of microcarrier for T cells, which are naturally non-adherent.
\subsection{overview of T cells in immunotherapies} \subsection{overview of T cells in immunotherapies}
% all numbers reflect the citation index in my review paper
One of the first successful T cell-based immunotherapies against cancer is One of the first successful T cell-based immunotherapies against cancer is
\glspl{til}\cite{Rosenberg2015}. This method works by taking tumor specimens \glspl{til}\cite{Rosenberg2015}. This method works by taking tumor specimens
from a patient, allowing the tumor-reactive lymphocytes to expand \exvivo{}, and from a patient, allowing the tumor-reactive lymphocytes to expand \exvivo{}, and
@ -746,6 +745,48 @@ compared to state-of-the-art systems.
\subsection{cell sources in T cell manufacturing} \subsection{cell sources in T cell manufacturing}
T cells for cell manufacturing can be obtained broadly via two paradigms:
autologous and allogeneic. The former involves obtaining T cells from a patient
and giving them back to the same patient after \exvivo{} expansion and genetic
modification. The latter involves taking T cells from a (usually) healthy donor,
expanding them and manipulating them as desired, storing them long term, and
then giving them to multiple patients. There are advantages and disadvantages to
both, and in some cases such as \gls{til} therapy, the only option is to use
autologous therapy.
Autologous T cells by default are much safer. By definition, they will have no
cross-reactivity with the patient and thus \gls{gvhd} is not a
concern\cite{Decker2012}. However, there are numerous disadvantages. Autologous
therapies are over 20X more costly as the process needs to be repeated for every
patient\cite{Harrison2019}. To highlight how resource-intensive this can be,
many cell products are manufactured at a centralized location, so patient T
cells need to be shipped twice on dry ice from the hospital and back. In
additional to being expensive, this can add days to the process, which is
critical for patients with fast moving diseases. Manufacturing could be done
on-site in a decentralized manner, but this requires more equipment and
personnel overall. Using cells from a diseased patient has many drawbacks in
itself. Cancer patients (especially those with chronic illnesses) often have
exhausted T cells which expand far less readily and are consequently less
potent\cite{Wherry2015, Ando2019, Zheng2017}. Additionally, they may have high
frequencies of T\textsubscript{reg} cells which inhibitory\cite{Decker2012}.
Removing these cells as well as purifying Th1 cells may enhance the potency of
the final product\cite{Goldstein2012, Drela2004, Rankin2003, Luheshi2013,
Grotz2015}; however, this would make the overall process more expensive as an
additional step would be required.
Allogeneic T cell therapies overcome nearly all of these disadvantages. Donor
\glspl{pbmc} are easy to obtain, they can be processed in centralized locations,
they can be stored easily under liquid nitrogen, and donors could be screened to
find those with optimal anti-tumor cells. The key is overcoming \gls{gvhd}.
Obviously this could be done the same way as done for transplants where patients
find a `match' for their \gls{hla} type, but this severally limits options. This
can be overcome by using gene-editing (eg \glspl{zfn}, \glspl{talen}, or
\gls{crispr} to remove the native \gls{tcr} which would prevent the donor T
cells from attacking host tissue\cite{Liu2019, Wiebking2020, Provasi2012,
Berdien2014, Themeli2015}. To date there are about 10 open clinical trials
utilizing allogeneic T cell therapies edited with \gls{crispr} to reduce the
likelihood of \gls{gvhd}.
\subsection{methods to scale T cells} \subsection{methods to scale T cells}
In order to scale T cell therapies to meet clinical demands, automation and In order to scale T cell therapies to meet clinical demands, automation and