ebook img

Interaction of immune and cancer cells PDF

358 Pages·2022·6.898 MB·English
Save to my drive
Quick download
Download
Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.

Preview Interaction of immune and cancer cells

Experientia Supplementum 113 Magdalena Klink Izabela Szulc-Kielbik   Editors Interaction of Immune and Cancer Cells Second Edition Experientia Supplementum Volume 113 Experientia Supplementum (EXS) is a multidisciplinary book series originally cre- atedasasupplementtothejournalExperientiawhichappearsnowunderthecover ofCellularandMolecularLifeSciences. Theeditedvolumesfocusonselectedtopicsofbiologicalorbiomedicalresearch, discussingcurrentmethodologies,technologicalinnovations,noveltoolsandappli- cations,newdevelopmentsandrecentfindings. * * * Theseriesisavaluablesourceofinformationnotonlyforscientistsandgraduate studentsinmedical,pharmacologicalandbiologicalresearch,butalsoforphysicians aswellaspractitionersinindustry. EXSisindexedinMedlineandChemicalAbstractService(CAS). * * * Moreinformationaboutthisseriesathttps://link.springer.com/bookseries/4822 (cid:129) Magdalena Klink Izabela Szulc-Kielbik Editors Interaction of Immune and Cancer Cells Second Edition Editors MagdalenaKlink IzabelaSzulc-Kielbik InstituteofMedicalBiology InstituteofMedicalBiology PolishAcademyofSciences PolishAcademyofSciences Lodz,Poland Lodz,Poland ISSN1664-431X ISSN2504-3692 (electronic) ExperientiaSupplementum ISBN978-3-030-91310-6 ISBN978-3-030-91311-3 (eBook) https://doi.org/10.1007/978-3-030-91311-3 ©TheEditor(s)(ifapplicable)andTheAuthor(s),underexclusivelicensetoSpringerNatureSwitzerland AG2022 Thisworkissubjecttocopyright.AllrightsaresolelyandexclusivelylicensedbythePublisher,whether thewholeorpartofthematerialisconcerned,specificallytherightsoftranslation,reprinting,reuseof illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similarordissimilarmethodologynowknownorhereafterdeveloped. Theuseofgeneraldescriptivenames,registerednames,trademarks,servicemarks,etc.inthispublication doesnotimply,evenintheabsenceofaspecificstatement,thatsuchnamesareexemptfromtherelevant protectivelawsandregulationsandthereforefreeforgeneraluse. The publisher, the authors, and the editorsare safeto assume that the adviceand informationin this bookarebelievedtobetrueandaccurateatthedateofpublication.Neitherthepublishernortheauthorsor theeditorsgiveawarranty,expressedorimplied,withrespecttothematerialcontainedhereinorforany errorsoromissionsthatmayhavebeenmade.Thepublisherremainsneutralwithregardtojurisdictional claimsinpublishedmapsandinstitutionalaffiliations. ThisSpringerimprintispublishedbytheregisteredcompanySpringerNatureSwitzerlandAG. Theregisteredcompanyaddressis:Gewerbestrasse11,6330Cham,Switzerland Preface Themicroenvironmentofsolidtumorisacomplexstructureconsistingofahetero- geneous population of tumor cells and various non-tumor cells including immune cells,fibroblast,mesenchymalcells,endothelialcells,stemcells,andothers.More- over, the tumor microenvironment (TME) also contains extracellular matrix pro- teins, soluble factors (i.e., chemokines and cytokines), extracellular vesicles, and vascularandlymphaticnetworks.Everyelementofthiscomplexstructurestrongly affectsthemalignantcells’growth,survival,andabilitytometastasize.Thedynamic processesoccurringinTMEbetweentumorandnon-tumorcells,aswellasstromal factors,are known as cancer immunoediting which consists of three phases:elimi- nation, equilibrium, and escape. However, a full understanding of the mechanisms underlying tumor progression requires the thorough study of abovementioned fac- torsandcellswithinTME. The first purpose of this book is to present current knowledge and the most importantaspectsofinteractionsbetweenseveraltypesofcellspresentintheTME. Infiltrating immune cells such as various subsets of lymphocytes, dendritic cells, macrophages,neutrophils,naturalkillercells,andmyeloid-derivedsuppressorcells are the most important players involved in a cross talk with the tumor cells. Depending on the phenotype and repertoire of secreting signals, these cells can either suppress or promote tumor growth and metastasis. Moreover, the tumor- infiltrating lymphocytes, macrophages, and neutrophils are potential prognostic or predictivebiomarkersincancerandarealsocomponentsofapromisingtherapeutic strategy.Anotherimportantelement,takingpartintumordevelopmentandprogres- sion,isstromaltissuewhichconsistsoffibroblasts,myofibroblasts,endothelialcells, and extracellular matrix proteins. The stromal cells, mainly fibroblasts, secrete variousfactors(e.g.,transforminggrowthfactorβ)thataffecttumorcellsandresult inamoreaggressivecancerphenotype.Currently,themainfocusisoncancerstem cells also known as tumor-propagating cells which are capable of self-renewal, whichisanimportantmechanismoftumorproliferation,differentiation,metastasis, andchemoresistance.Ingeneral,theimmuneandnon-immunecellsaswellasother components of TME (cytokines/chemokines, growth factors, and extracellular v vi Preface vehicles)arethebestknowntoparticipatein(i)developmentofimmunosuppression ofadaptiveimmunity,(ii)inductionofepithelial–mesenchymaltransitionofcancer cellsallowingthemtoleaveprimarytumorandcolonizesecondarysites,(iii)stromal remodeling,(iv)angiogenesis,and(v)cancerescapefromimmunosurveillance. Thesecondaimofthisbookistofocusonthecurrentlyongoingpreclinicaland clinical studies concerning immunotherapy. The most advanced research concerns targeted therapy to immune checkpoints, the cytotoxic T lymphocyte-associated antigen 4 and anti-programmed cell death protein 1. What is more, the full human monoclonalantibodiesagainstthesebothproteins(ipilimumabandnivolumab)are approved for the treatment of metastatic melanoma and are further extensively studied in other malignant diseases. Another promising approach for immunother- apy is the one based on the adoptive transfer of autologous tumor-specific T lymphocytes or genetically engineered T cells that express an exogenous cancer- specificT-cellreceptor orchimericantigenreceptor.Thethirdstrategyisbased on dendritic cells. The most studied are methods concerning the targeting of lectin/ scavengerreceptorsorusingtumorantigen-loadeddendriticcellsasavaccine. Presentedcollectiveworkfeaturesthecomprehensivesummaryoftheinteraction betweenvarioustypesofcellspresentinthesolidtumormicroenvironmentaswell as the most advanced strategies of immunotherapy. This second edition of previ- ously published book is strongly updated and expanded with two new chapters describing stem cells and natural killer cells. We hope that the presented work is describing, in sufficient detail, why tumor cells can survive and spread in the host organism, despite of anti-tumor activity of immune cells, and how the activity of immunecellscanbeusedtodevelopanticancertherapeuticstrategies. Finally,wewouldliketotakeanopportunitytoexpressourgratitudeforallthe authorswhohavecontributedtothisvolume.Theirvastknowledgeandexperience inthefieldoftumormicroenvironmentmadethecreationofthisbookpossible. Lodz,Poland MagdalenaKlink July,2021 IzabelaSzulc-Kielbik Contents 1 CancerImmunoediting:Elimination,Equilibrium, andImmuneEscapeinSolidTumors. . . . . . . . . . . . . . . . . . . . . . . 1 JacekR.WilczyńskiandMarekNowak 1.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 1.2 ImmunosurveillanceoftheHostAgainst Cancer—Elimination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 1.3 CancerDormancyandCancer-ImmuneEquilibrium. . . . . . . . . 6 1.4 CancerEscapeMechanisms. . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1.4.1 DisruptionoftheAntigen-PresentingMachinery, HLA-G,andCostimulatoryMolecules. . . . . . . . . . . . . 10 1.4.2 Tumor-InfiltratingLymphocytesandImmune Escape. . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . .. . . . 14 1.4.3 ImmunoregulatoryFunctionofTumor-Associated MyeloidCells(TAMCs). . . . . . . . . . . . . . . . . . . . . . . 19 1.4.4 DendriticCellsasTumorGrowthEnhancers. . . . . . . . 25 1.4.5 InflammationandCancerEscape. . . . . . . . . . . . . . . . . 27 1.4.6 ResistancetoApoptosisandTumor “CounterAttack”. . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 1.4.7 TheRoleofTumorStromainImmuneEscape. . . . . . . 37 1.4.8 MicrovesiclesandExosomes—Mediators ofTumorEscape. . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 1.5 Conclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 2 Tumor:StromaInteractionandCancer. . . . . . . . . . . . . . . . . . . . . 59 MichaelP.Rogers,ZhiyongMi,NeillY.Li,PhilipY.Wai, andPaulC.Kuo 2.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 2.2 TME:TheNonimmuneComponents. . . . . . . . . . . . . . . . . . . . 62 2.2.1 EpithelialCells. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 vii viii Contents 2.2.2 BasementMembraneandExtracellularMatrix. . . . . . . 63 2.3 TME:TheImmuneComponents,ChronicInflammation, WoundHealing,andTumorProgression. . . . . . . . . . . . . . . . . 64 2.4 EMTandTGF-β. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 2.4.1 TGF-βSignaling. . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 2.5 OsteopontinandEMT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 2.6 Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 3 Tumor-InfiltratingLymphocytesandTheirRoleinSolid TumorProgression. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 TheresaL.Whiteside 3.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 3.2 StudiesoftheIntratumorImmuneLandscape. . . . . . . . . . . . . . 92 3.3 ImmuneScoreintheTME. . . .. . . .. . . .. . . .. . . .. . .. . . .. 94 3.4 AntitumorEffectsofTIL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 3.4.1 CD8+CytolyticTCells. . . . . . . . . . . . . . . . . . . . . . . 95 3.4.2 CD4+HelperTCells. . . . . . . . . . . . . . . . . . . . . . . . . 97 3.4.3 RegulatoryTCells(Treg). . . . . . . . . . . . . . . . . . . . . . 98 3.4.4 BCells. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 3.4.5 NaturalKiller(NK)Cells. . . . . . . . . . . . . . . . . . . . . . 100 3.5 SummaryandConclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . 101 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 4 Tumor-AssociatedMacrophages:ReasonstoBeCheerful, ReasonstoBeFearful. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 IzabelaSzulc-KielbikandMichalKielbik 4.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 4.2 ClassificationofMacrophages. . . . . . . . . . . . . . . . . . . . . . . . . 110 4.3 CharacterizationofTumor-AssociatedMacrophages. . . . . . . . . 113 4.4 RoleofTAMsinCancerInitiation,Promotion, andProgression. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116 4.4.1 TAMsinChronicInflammation. .. . . .. . .. . . .. . . .. 116 4.4.2 TAMsinMetastasisandPremetastaticNiche. . . . . . . . 117 4.4.3 TAMsinAngiogenesis. . . . . . . . . . . . . . . . . . . . . . . . 119 4.4.4 TAMsinAntitumorImmuneResponseSuppression. . . 121 4.5 TAMsinCancerTherapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . 122 4.6 TherapeuticApproachesofTargetingTAMs—From ExperimentationtoClinicalTrials. . . . . . . . . . . . . . . . . . . . . . 124 4.7 Conclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 5 PolymorphonuclearNeutrophilsandTumors:FriendorFoe?. . . . 141 IzabelaSzulc-KielbikandMagdalenaKlink 5.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 5.2 CharacterizationofTumor-AssociatedNeutrophils. . . . . . . . . . 143 Contents ix 5.2.1 RequirementofNeutrophilstotheTumorTissue. . . . . 143 5.2.2 HeterogeneityofTumor-AssociatedNeutrophils. . . . . . 144 5.3 DualRoleofTANsinTME. . . . . . . . . . . . . . . . . . . . . . . . . . 146 5.4 AntitumoralEffectofTANs. . . . . . . . . . . . . . . . . . . . . . . . . . 147 5.4.1 ROSProduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 5.4.2 Fas/FasLSystem. . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 5.4.3 Trail. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 5.4.4 Antibody-DependentCell-MediatedCytotoxicity (ADCC). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150 5.5 ProtumoralEffectsofTANs. . . . . . . . . . . . . . . . . . . . . . . . . . 151 5.5.1 NeutrophilElastase(NE). . . . . . . . . . . . . . . . . . . . . . 151 5.5.2 MatrixMetalloproteinase-9(MMP-9). . . . . . . . . . . . . 153 5.5.3 OncostatinM(OSM). . . . . . . . . . . . . . . . . . . . . . . . . 153 5.5.4 CathepsinG(CG). . . . . . . . . . . . . . . . . . . . . . . . . . . 154 5.5.5 Arginase1(ARG-1). . . . . . . . . . . . . . . . . . . . . . . . . . 154 5.5.6 PD-L1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 5.5.7 NeutrophilsExtracellularTraps(NETs). . . . . . . . . . . . 156 5.5.8 TumorCellExtravasation. . . . . . . . . . . . . . . . . . . . . . 157 5.6 Conclusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159 6 RoleofNKCellsinTumorProgression. . . . . . . . . . . . . . . . . . . . . 169 IñigoTerrénandFranciscoBorrego 6.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170 6.2 NKCellBiology. . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . 171 6.2.1 NKCellDiversity. . . . . . . . . . . . . . . . . . . . . . . . . . . 171 6.2.2 NKCellEffectorFunctions. . . . . .. . . . . . . . . . . . . . . 172 6.3 MechanismsofTumorResistancetoNKCell–Mediated Killing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 174 6.4 NKCellsinTumorProgression. . . . . . . . . . . . . . . . . . . . . . . . 177 6.4.1 NKCellInfiltrationintheTME. . . . . . . . . . . . . . . . . 177 6.4.2 PhenotypeofTINKCells. . . . . . . . . . . . . . . . . . . . . . 178 6.4.3 PrognosticValueofNKCells. . . . . . . . . . . . . . . . . . . 179 6.5 ConcludingRemarks. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180 7 TheRoleofMyeloid-DerivedSuppressorCellsinTumor GrowthandMetastasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189 DefneBayik,JuyeunLee,andJustinD.Lathia 7.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 7.1.1 MDSCSubsets.. . . . .. . . . .. . . .. . . . .. . . . .. . . .. 191 7.1.2 LineageRelationshipofMDSCs. . . . . . . . . . . . . . . . . 193 7.1.3 MDSCsinCancer. . . . . . . . . . . . . . . . . . . . . . . . . . . 196 7.2 SignalingNetworksDrivingMDSCsinCancer. . . . . . . . . . . . . 197 7.2.1 Recruitment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197 7.2.2 MaintenanceandFunction. . . . . . . . . . . . . . . . . . . . . 200

See more

The list of books you might like

Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.