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how can a tumor evade the immune system
it can loose the antigen that alerted the immune system (antigen loss variants), it can loose the antigen processing molecules (MHC molecules on the surface), it can down regulate the MHC, is can secrete immunosuppressive proteins, it can express Fas L, it can induce Tregs, it can induce myeoloid derived suppressor cells (MDSC); this is all just like what a bac or virus would do to evade
Mage-1 or MART-1
among the first human tumor antigens cloned; stands for melanoma antigen 1 or melanoma antigen recognized by T cells 1
the major thing that is recognized in these tumor cells
over expressed normal self genes making too many normal self peptides
TAA (tumor associated antigens) ID methods
cDNA libraries (requires specific T cells); SEREX (serological analysis of recombinant cDNA expression libraries) (requires specific antibodies); 2D-PAGE/mass spec (proteomics) (requires specific antibodies); reverse immunology= subtraction hybridization, phage display libraries, peptide elution form MHC class I, serial analysis of gene expression (SAGE), differential display RT-PCR
immune responses against tumors
T cells are the primary effectors against solid tumors; NK and NK-T cells may be important for killing MHC class-I negative tumors; an active role for B cells or antibodies has been demonstrated (passive administration of specific mAb) used to treat some cancers; immune checkpoint blockade); an active role for macrophages has been demonstrated
induction of T cell responses to tumors
induction of CTLs usually requires cross priming of T cells by DCs; most tumors lack co stimulatory molecules, an exception is B cell lymphoma; cross priming is the basis for ex vivo DC based tumor vaccines; T cell responses can be induced via vaccination using TAA so antigens are cross presented
a role of NK cells
MHC-I is inhibitory to NK cells; so MHC-I negative tumors may then be susceptible to NK cell killing (why would they try to get rid of their MHC-I? to evade the CD8 T cells
categories of tumor immunotherapy
passive (short term therapy that has a half life)= administration of monoclonal antibody (FDA approved therapy), systemic cytokines, adoptive cell therapy (ACT)(T cell transfer); active (confers immunity for a lifetime)= vaccines (represent the majority of clinical trials several near FDA approval, one approved 2010)
CTLA-4 and PD-1 checkpoint blockade to induce effector T cell function
you give the pt antibodies against CTLA-4 and PD1 so that they are blocked and the T cell always becomes effector and does its thing (CTLA-4 and PD-1 (co inhibitory signals) usually used to stop the cell from reacting to self cells); checkpoint blocking allows a sustained T cell response to include an increase in inflammatory and effector cytokine production
adoptive cell therapy (ACT)
grab T cells from a pt with cancer, test them to find some that attack the cancer cells (in culture) then proliferate them and give them back to the pt; can take this a step further and destroy all their other T cells (lymphodepletion) so that you can pump them pull of these specific T cells
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