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Michael Gerner
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E-mail: gerne002@umn.edu
Thesis Advisor: Matt
Mescher
Year entered: 2003
Degrees received:
B.S., Biochemistry, University of Wisconsin, Madison, Wisconsin
1998
Honors and Awards:
- Cancer Biology Training Grant 2005
Thesis research:
Immunosuppression is one of hallmarks of cancer progression,
understanding the mechanisms of which can lead to enhancing
current therapy design. We examined the responses of naïve
CD4 and CD8 T cells to subcutaneous tumors and found that
CD8 T cells were being activated by immature CD8a+ DC presenting
tumor-specific proteins in the draining LN. However, the CD8
T cells were tolerized and did not affect tumor growth. In
sharp contrast, CD4 T cells remained ignorant and did not
exhibit helper activity throughout disease progression. These
differences in T cell activation were due to tumor-mediated
inhibition of antigen uptake by tumor infiltrating DC and
poor subsequent migration to draining LN. These results point
to a novel mechanism of cancer immunosuppression, where inhibition
of DC mediated CD4 T cell activation prevents CD4 T cell anti-tumor
activity and does not allow for CD4 T cell help for CD8 T
cell responses.
Publications:
- 2. Gerner, M.Y., Casey K.A., Mescher M.F. Defective MHC-II
presentation by DC limits CD4 T cell help for anti-tumor
CD8 T cell responses. In Press (J Immunol).
- Mescher, M. F., F. E. Popescu, M. Gerner, C. D. Hammerbeck,
and J. M. Curtsinger. 2007. Activation-induced non-responsiveness
(anergy) limits CD8 T cell responses to tumors. Semin
Cancer Biol 17:299-308.
- Mescher MF, Curtsinger JM, Agarwal P, Casey KA, Gemer
M, Hammerbeck CD, Popescu F, Xiao ZG. 2006. Signals required
for programming effector and memory development by CD8(+)
T cells. Immunol
Rev. Jun;211:81-92. Review.
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