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These data ... that oncogenic EGFR signaling remodels the tumor microenvironmentto triggerimmune escape
to develop a mechanism - based vaccineto preventHNSCC immune escape
If vaccine - induced T - cell responsesledto immune escape
Proteins)(+ ) dendritic cells within the tumor microenvironment dominantly resists the effector phase of an anti - tumor T cell responsecontributingto immune escape
Thyagarajan Hepatitis B virus ( HBV ) surface antigen mutationsmay leadto immune escape
ITGAE Antibodies)(+ ) dendritic cells within the tumor microenvironment dominantly resists the effector phase of an anti - tumor T cell responsecontributingto immune escape
Xin - Hua Li Article : N - Glycosylation Mutations within Hepatitis B Virus Surface Major Hydrophilic RegionContribute Mostlyto Immune Escape
Yu , DM , et al . N - glycosylation mutations within hepatitis B virus surface major hydrophilic regioncontribute mostlyto immune escape
Lack of Batf3 / CD103(+ ) dendritic cells within the tumor microenvironment dominantly resists the effector phase of an anti - tumor T cell responsecontributingto immune escape
Ecorse temporally distinct pd - l1 expression by tumor and host cellscontributesto immune escape
AbstractThe variability of the hepatitis C virus ( HCVcontributesto immune escape
Lack of Batf3 / CD103 ( zeige ITGAE Proteine)(+ ) dendritic cells within the tumor microenvironment dominantly resists the effector phase of an anti - tumor T cell responsecontributingto immune escape
Genetic lesions that target HLA - A , HLA - B , HLA - C or CD58leadto immune escape
any mutation at p9leadsto immune escape
Inflammatory Cytokine - Induced Adaptive Immune ResistanceThe production of proinflammatory cytokines by tumor - infiltrating cells ... the cancer cellsmay leadto immune escape
I complex and antigen presentationthus contributingto immune escape
Several mechanisms by whichcontributesto immune escape
the exact mechanisms by whichleadto immune escape
multiple mechanismscontributingto immune escape
authors Mikhail M. Dikov Activation of Notch signaling in hematopoietic cells by tumorscontributesto immune escape
Yu DM , Li XH , Mom V , Lu ZH , Liao XW , Han Y , Pichoud C , Gong QM , Zhang DH , Zhang Y , et al . N - glycosylation mutations within hepatitis B virus surface major hydrophilic regioncontribute mostlyto immune escape
high rates of mutation(passive) caused byimmune escape
response to ICB Antigen presentation deficiencymay leadto immune escape
tumour - induced dysfunction of T cell clones ... a tumour evasion mechanismcontributesto immune escape
Multiple defects in HLA class I antigen presentationmay contributeto immune escape
mechanisms that could potentially be targetedto preventimmune escape
H Suen , R Brown , S Yang , C Weatherburn , P J Ho , N Woodland , N Nassif , P Barbaro , C Bryant , D Hart , J Gibson , D Joshua Tumour - induced dysfunction of cytotoxic T cells in patients with multiple myeloma ( MMmay contributeto immune escape
structural variations ( SVs ) commonly disrupting the 3′ region of the PD - L1 gene(passive) caused byimmune escape
when expression of the neoantigen was warranted in all tumor cells or when additional immunotherapeutic means such as irradiation were applied(passive) was preventedImmune escape
the tumor microenvironment of PMBCL ... surface moleculescontributeto immune escape
CAFs , which express fibroblast activation protein ( FAPcontributeto immune escape
In contrast , tumor cells highly express PD - L1 , which binds to receptor PD-1 expressed on activated T cellsleadingto immune escape
The cytokine GM - CSF , which is used to enhance white cell counts in many cancer patients , also expands a population of immune - suppressive monocytic cells that can block the entry of activated antitumor T cells into the tumor microenvironmentcontributingto immune escape
thereby necessitating the use of either multiple Ags , or cross - reactive self - antigensto preventimmune escape
In HBV infection , responses to HBV nucleocapsid antigens , usually associated with immune clearancemay leadto immune escape
the anti - tumor immune response , including high levels of suppressive intratumoral cytokines , the constitutive or induced expression of immune checkpoint molecules by the tumor cells , various other phenotypic alterationsleadto immune escape
as many mutation messages as possible that can function to elicit robust anti - tumour effects and that are less likelyto triggerimmune escape
Hepatitis C Virus Hypervariable Region 1 Modulates Receptor Interactions , Conceals the CD81 Binding Site , and Protects Conserved Neutralizing Epitopes Bankwitz , D. , Steinmann , E. , Bitzegeio , J. , Ciesek , S. , Friesland , M. , Herrmann , E. , Zeisel , M. B. , Baumert , T. F. , Keck , Z. , Foung , S. K. , Pecheur , E. , Pietschmann , T. 2010 ; 84 ( 11 ) : 5751 - 5763 The variability of the hepatitis C virus ( HCVcontributesto immune escape
that the absence of CD103 + DCs within the tumour microenvironment resists the effector phase of an anti - tumour T cell responsecontributingto immune escape
Fingerprint Dive into the research topics of ' Combination immunotherapy with α - CTLA-4 and α - PD - L1 antibody blockadepreventsimmune escape
immunologic tumor rejectionpreventimmunologic tumor rejection
in aggressive ovarian cancersresultingin aggressive ovarian cancers
immune escape from occurring by eliminating appropriate escape epitopes from compositions intended to be used as vaccinesto preventimmune escape from occurring by eliminating appropriate escape epitopes from compositions intended to be used as vaccines
in the maintenance of relatively lower viral loads and clinical advantage [ 17 ] [ 20 ] , [ 21may ... resultin the maintenance of relatively lower viral loads and clinical advantage [ 17 ] [ 20 ] , [ 21
to a transmission dead - endleadsto a transmission dead - end
to the evolution of a subclass of PfEMP1 variants with a growth advantage in immunologically naïve hostsleadingto the evolution of a subclass of PfEMP1 variants with a growth advantage in immunologically naïve hosts
in no response to PD-1 mAb therapyresultingin no response to PD-1 mAb therapy
to increased antigen – hot andleadsto increased antigen – hot and
to poor tumor clearancecontributesto poor tumor clearance
in more efficient T - cell exhaustion in EBV+DLBCLresultingin more efficient T - cell exhaustion in EBV+DLBCL
to the severity of the outbreakcontributingto the severity of the outbreak
to loss of viral control in early HIV infectionmay contributeto loss of viral control in early HIV infection
disease relapse after haplo - HCTcausingdisease relapse after haplo - HCT
to persistence either by repeated selection of preexisting viruses or by the incorporation of advantageous mutations to generate new variantsmay contributeto persistence either by repeated selection of preexisting viruses or by the incorporation of advantageous mutations to generate new variants
to decreased expression of NKG2D on effector cellsleadingto decreased expression of NKG2D on effector cells
to the above drug developmentledto the above drug development
to the development of a clinically overt cancerleadingto the development of a clinically overt cancer
heritability of set - point virus load Between - host adaptation is only possible if spVL is inherited from one person to the nextcausesheritability of set - point virus load Between - host adaptation is only possible if spVL is inherited from one person to the next
to increased research into combination therapy with EGFR TKIs and immune checkpoint blockadeledto increased research into combination therapy with EGFR TKIs and immune checkpoint blockade
to viral persistencecontributesto viral persistence