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Volume 8, Issue 3 (Suppl)
J Clin Cell Immunol, an open access journal
ISSN: 2155-9899
Page 48
Notes:
conference
series
.com
June 29-July 01, 2017 Madrid, Spain
8
th
European
Immunology Conference
Euro Immunology 2017
June 29-July 01, 2017
The combination of disease modeling, immunological profiling and the NSG-UC animal model leads
to a better understanding of the mechanism underlying inflammation in UC
O
ne reason for the lack of individualized therapies in ulcerative colitis (UC) may be that the conventional approaches are
not adequate to understand the complexity of chronic inflammatory diseases. They mostly rely on the identification of
certain cell types and cytokines associated with the disease phenotype, followed by verification of their roles
in vitro
and
in
vivo
. This approach does not take into consideration that the observed pathologies might be the result of different causes.
In addition, inflammatory responses are highly dynamic processes that require the cross talk of the immune-, epithelial-,
endothelial-, muscle cells, and fibrocytes. The conventional approach further disregards the high plasticity of T-cells and
monocytes, which both have the capacity to adopt their phenotype depending on the inflammatory milieu. Therefore, we took
a more comprehensive approach and developed FACS, ELISA and autoantibody panels to portray individual inflammatory
profiles. In addition, we developed a disease map of UC by computational modeling. Finally, we developed an animal model
which enables us to proof the hypothesis generated by modeling and profiling. So far, we tested infliximab, adulizumab,
sirolimus, anti CD1a antibodies, anti CCR4 antibodies and the IL-4R
α
/IL-13
α
1 inhibitor pitrakinra in our mouse model.
Results suggest that the animal model is highly reflective of the human disease, that therapeutic responses can be predicted by
the computational model and that novel therapeutics emerge from this approach.
Biography
Roswitha Gropp has over 25 years of experience in preclinical development and inflammatory diseases. She recently took on a different view considering the inflammatory
process in UC as an uncontrolled wound healing process. This hypothesis assumes that epithelial damage induces the release of signals to evoke a Th2 characterized
inflammatory response that ultimately results in repair of the colon. Using agent based modeling first disease maps were developed to describe the inflammatory milieu and
the dynamics of the inflammatory response. This approach together with immunological profiling of patients allows for a better understanding of underlying mechanisms
ultimately leading to individualized therapies.
Roswitha.Gropp@med.uni-muenchen.deRoswitha Gropp
Hospital of the LMU, Germany
Roswitha Gropp, J Clin Cell Immunol 2017, 8:3(Suppl)
DOI: 10.4172/2155-9899-C1-035