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WhatWhat youyou needneed toto knowknow aboutabout innateinnate immunityimmunity

JenniferJennifer KoKo MD,MD, PhDPhD ClevelandCleveland ClinicClinic /PathologyImmunology/Pathology andand LaboratoryLaboratory MedicineMedicine InnateInnate ImmunityImmunity

 FirstFirst lineline ofof defense,defense, immediateimmediate defensedefense  DayDay toto dayday protectionprotection  OnlyOnly whenwhen innateinnate defensedefense bypassed,bypassed, evadedevaded oror overwhelmedoverwhelmed isis adaptiveadaptive immunityimmunity requiredrequired  NonNon--specificspecific  RecognizeRecognize pathogenspathogens inin aa genericgeneric wayway  DoesDoes notnot conferconfer longlong lastinglasting oror protectiveprotective immunityimmunity toto hosthost  EvolutionarilyEvolutionarily older,older, foundfound inin primitiveprimitive organismsorganisms

InnateInnate ImmunityImmunity andand InflammationInflammation

 1)1) RespondRespond rapidlyrapidly toto tissuetissue damagedamage  physicalphysical andand chemicalchemical barrierbarrier  recruitmentrecruitment ofof immuneimmune cellscells toto sitesite ofof injuryinjury  2)2) LimitLimit spreadspread ofof infectioninfection  identificationidentification andand removalremoval ofof foreignforeign substancessubstances  activationactivation ofof thethe complementcomplement cascadecascade  activationactivation ofof coagulationcoagulation cascadecascade  3)3) InitiateInitiate adaptiveadaptive immuneimmune responseresponse  antigenantigen presentationpresentation andand cytokinecytokine productionproduction  4)4) InitiateInitiate tissuetissue repairrepair InnateInnate ImmunityImmunity –– Physical/ChemicalPhysical/Chemical BarriersBarriers Breach of physical barrier  -“resting” innate immune cells become activated to kill microbes, secrete to recruit and activate additional leukocytes, and to promote systemic killing and removal of microbes. InnateInnate ImmunityImmunity-- 11stst respondersresponders InnateInnate ImmunityImmunity-- /MacrophagesMonocytes/

- MonocyteMonocyte --derivedderived macrophagesmacrophages ““largelarge eaterseaters ”” oror ,histiocytes, areare presentpresent inin allall tissuestissues - ““SentinelsSentinels ”” ofof immuneimmune systemsystem -- surveysurvey forfor ““foreignforeign ”” invadersinvaders - ForeignForeign microbesmicrobes areare recognizedrecognized viavia variousvarious cellcell surfacesurface andand intracellularintracellular receptorsreceptors - ReceptorReceptor ligationligation andand cytokinescytokines causescauses macrophagemacrophage activationactivation - ActivatedActivated macrophagesmacrophages - Digest and present from microbes - Produce , cytokines, other molecules to recruit other immune cells MacrophageMacrophage PhagocytosisPhagocytosis

Microbe killing= • + =

•Nitric oxide (nitric oxide synthase, iNOS2)

anion (NADPH oxidase, -Macrophages kill respiratory internalized microbes burst)

via reactive oxygen and •Hydrogen nitrogen species peroxide () Toll receptors are stimulated by Associated Molecular Patterns (PAMPs) NOD-like receptor (NLR) proteins are intracellular pattern recognition receptors (PRRs) Induced Innate Responses mediated by cytokines secreted by stimulated sentinel cells Chemokines secreted by stimulated sentinel cells recruit additional immune cells InnateInnate ImmunityImmunity--MacrophageMacrophage

Systemic Complement Inflammatory •MBL Cascade Response •TNF α •IL-6 •IL-1 •Pattern Recognition Receptors

•Toll-like receptors •NLRs • mannose receptor (clearance of •Macrophage •Scavenger chemokines/cytokines receptors microbes) •Co-stimulatory molecules •CD80/86 • •TNF α

•IL-8 Recruitment of other cells mediated vascular dilation and vascular permeability facilitate extravasation into infected tissues

-Macrophage activation causes degradation of membrane phospholipids and rapid production of prostaglandins, and -activating factor which act with cytokines directly on smooth muscle and endothelial cells Cytokine induced adhesion  cytokines and chemokines mediate neutrophil weak and firm adhesion to vascular InnateInnate ImmunityImmunity-- 11stst respondersresponders Neutrophils

 Essential to innate , hallmark of acute  Most prevalent WBC in with 50-100 billion produced per day  55% weight dedicated  Migrate in response to IL-8, C5a, leukotrienes, fMLP via  Circulate 5.4 days, live in 1-2 days  Limit propagation of certain  Limit host damage due to inflammation  Phagocytosed by macrophages after pathogen digestion Neutrophil NET formation InnateInnate ImmunityImmunity--MacrophageMacrophage

Systemic Complement Inflammatory •MBL Cascade Response •TNF α •IL-6 •IL-1 •Pattern Recognition Receptors

•Toll-like receptors •NLRs •Macrophage Phagocytosis mannose receptor (clearance of •Macrophage •Scavenger chemokines/cytokines receptors microbes) •Co-stimulatory molecules •CD80/86 •Neutrophils •TNF α

•IL-8 Recruitment NETosis of other cells Cytokines from PAMP-stimulated sentinel cells stimulate the production of acute phase proteins, which opsonize a large spectrum of pathogens bearing common pathogen associated molecular patterns There are two innate mechanisms by which complement can be activated: the pathway and the alternative pathway Complement feeds forward to activate and increase macrophage and neutrophil phagocytosis Complement can form the membrane attack complex, which leads to the lysis of target pathogens The spread of is limited by the response Viral nucleic acids stimulate the production of interferon by the infected , which mediates both autocrine and paracrine protective responses InnateInnate ImmunityImmunity-- 11stst respondersresponders NK cells

•Overlap innate and adaptive immunity •Stimulated by Type I •Kill cells with down-regulated MHC I expression •Down-regulated by viruses and tumors trying to avoid CD8+ T-cell killing •Kill “non-self” via mostly shared mechanisms with cytotoxic T-cells •TRAIL •GranzymeB •Perforin InnateInnate ImmunityImmunity andand InflammationInflammation

 1)1) RespondRespond rapidlyrapidly toto tissuetissue damagedamage  physicalphysical andand chemicalchemical barrierbarrier  recruitmentrecruitment ofof immuneimmune cellscells toto sitesite ofof injuryinjury  2)2) LimitLimit spreadspread ofof infectioninfection  identificationidentification andand removalremoval ofof foreignforeign substancessubstances  activationactivation ofof thethe complementcomplement cascadecascade  activationactivation ofof coagulationcoagulation cascadecascade  3)3) InitiateInitiate adaptiveadaptive immuneimmune responseresponse  antigenantigen presentationpresentation andand cytokinecytokine productionproduction  4)4) InitiateInitiate tissuetissue repairrepair Adaptive response initiation: presentation to T cells The context in which macrophage-derived dendritic cells present antigen to T-cells determines the type of adaptive response that follows

 ImmuneImmune surveillancesurveillance inin cancercancer  CarcinogenCarcinogen--inducedinduced tumorstumors arisearise moremore frequentlyfrequently andand quicklyquickly inin immunodeficientimmunodeficient micemice  CancerCancer cellscells thatthat arisearise inin immunodeficientimmunodeficient micemice areare inefficientinefficient atat initiatinginitiating secondarysecondary tumorstumors inin syngeneicsyngeneic immunocompetentimmunocompetent micemice  ImmuneImmune surveillancesurveillance inin cancercancer  HeavyHeavy CTLCTL andand NKNK cellcell infiltrationinfiltration predictspredicts improvedimproved outcomeoutcome inin severalseveral humanhuman tumorstumors  ImmunosuppressedImmunosuppressed organorgan transplanttransplant recipientsrecipients developdevelop donordonor --derivedderived cancercancer fromfrom ostensiblyostensibly tumortumor --freefree donorsdonors  ImmuneImmune escapeescape inin cancercancer  ClinicallyClinically apparentapparent tumorstumors variablyvariably suppresssuppress thethe antianti --tumortumor immuneimmune responseresponse  TumorTumor --associatedassociated inflammationinflammation cancan enhanceenhance tumortumor progressionprogression Immunoediting Normal Cells •Inflammation/radiation/carcinogens/viruses

Transformed Cells Protection •Tumor antigens/peptide-MHC I/ MHCII cross-presentation/NKG2D

3) Escape/Tumor Progression 1) Elimination/Immunosurveillance •T regulatory cells – IL-10 and TGF β •IFN γ and •Tumor-derived cytokines, growth IFN α/β factors, chemokines •Perforin •Trail •Myeloid-derived suppressor •Th1 and T c T cells, NKT, NK, cells (MDSC) γ δT cells 2) Equilibrium/Tumor Persistence

•Genetic instability and immune selection •Tumor variants •Immune exhaustion/inhibition

•Tumors may remain dormant Adapted from Dunn G et al, Nat Rev Immunol 6, 836-48 (2006). ChronicChronic InflammationInflammation hashas aa knownknown rolerole inin cancercancer initiationinitiation

 Tobacco,Tobacco, asbestosasbestos  BronchialBronchial CACA  AlcoholAlcohol  HepatocellularHepatocellular CA,CA, GastricGastric CA,CA, PancreaticPancreatic CACA  HelicobacterHelicobacter pyloripylori  MALTMALT lymphomalymphoma  ShistosomaShistosoma  bladderbladder CACA  HCVHCV  HepatocellularHepatocellular CACA  HPVHPV  CervicalCervical CACA  EndogenousEndogenous inflammationinflammation inin inflammatoryinflammatory bowelbowel diseadiseasese  ColonColon CACA  Barrett'sBarrett's esophagusesophagus  EsophagealEsophageal CACA -Scale largely tipped to pro-tumor effect of macrophages in established cancers

nature immunology volume 11 number 10 october 2010 MacrophageMacrophage andand chemotherapychemotherapy

 TAMTAM modulatemodulate responsesresponses toto chemotherapychemotherapy  MacrophagesMacrophages andand DCsDCs areare knownknown toto mediatemediate ‘‘‘‘ immunogenicimmunogenic cellcell deathdeath ’’’’ (ICD)(ICD) whichwhich somesome chemotherapieschemotherapies induceinduce inin somesome tumortumor modelsmodels  release of ‘‘ eat -me ’’ signals (e.g. ATP and high -mobility group B1 [HMGB1]) from dying tumor cells enhanced by some  activation and enhancement of their APC capacity and promotion of T cell responses against immunogenic tumors  AntitumorAntitumor activityactivity ofof somesome cytotoxiccytotoxic agentsagents maymay depdependend onon theirtheir abilityability toto reprogramreprogram propro --tumoraltumoral macrophagesmacrophages MacrophageMacrophage andand chemotherapychemotherapy

 TAMTAM depletiondepletion (anti(anti --CSF1CSF1 )antibodies) enhancesenhances thethe efficacyefficacy ofof somesome combinationcombination chemotherapychemotherapy  cyclophosphamide, methotrexate, and 5 -fluorouracil in chemoresistant, human breast cancer xenografts in immunodeficient mice  Paclitaxel in immunocompetent mice via increased anti -tumor CD8+ T - cell responses when macrophages were depleted  MacrophageMacrophage --derivedderived cathepsinscathepsins protectprotect cancercancer cellscells fromfrom thethe directdirect cytotoxiccytotoxic effectseffects ofof severalseveral chemotherapeutichemotherapeuticscs  CathepsinB  IL -1b  IL -17  blunted chemo effect  MacrophageMacrophage --derivedderived factorsfactors activateactivate STAT3STAT3 inin cancercancer stemstem cellscells toto promotepromote chemoresistancechemoresistance  UltimateUltimate effecteffect maymay dependdepend onon tumortumor immunogenicity,immunogenicity, sensitivitysensitivity ofof macrophagesmacrophages toto drug,drug, andand thethe inhereninherentt statestate ofof thth ee macrophagesmacrophages inin thethe particularparticular tumortumor MacrophagesMacrophages initiateinitiate aa woundwound reparativereparative programprogram thatthat enhancesenhances tumortumor regrowthregrowth NeutrophilNeutrophil

Potential Reality

 TumorTumor cellcell  GenotoxicityGenotoxicity associatedassociated withwith neutrophilneutrophil killingkilling ROSROS maymay initiateinitiate cancercancer throughthrough  ,Neutrophilia, andand highhigh reactivereactive neutrophil:lymphocyteneutrophil: (N:L)(N:L) ratioratio oxygenoxygen associatedassociated withwith poorpoor outcomeoutcome inin multiplemultiple species???species??? tumortumor typestypes  PromotePromote angiogenesisangiogenesis  AntiAnti --tumortumor TT --cellcell suppressionsuppression  TumorTumor cellcell migration,migration, invasioninvasion andand metastasismetastasis NK cells

 Prevent tumor progression  Immunosurveillance  Elimination phase  Cell stress  Non-self (low or absent MHC I)  Prevent tumor metastasis  Attack tumor emboli in the lungs  NK cell tumor targeting can be inhibited by  “Pseudo-self” Oncoimmunology. 2012 July 1; 1(4): 557–559. SummarySummary

 FunctionFunction ofof InnateInnate ImmunityImmunity  1) Respond rapidly to tissue damage  2) Limit spread of  3) Initiate adaptive  4) Initiate tissue repair  InnateInnate ImmunityImmunity inin CancerCancer  NeutrophilsNeutrophils  Promote tumor initiation  Promote tumor spread  MacrophagesMacrophages  Pro and anti - tumor effects in tumor initiation  Promote tumor spread  NKNK cellscells  Inhibit tumor initiation  Inhibit tumor spread Questions?Questions? 1) What is the importance of innate immunity in cancer?

 A) Innate immunity initiates malignant transformation via neutrophil-derived genotoxic stress  B) Innate immunity eradicates transformed tumor cells via NK recognition of non-self or cell stress  C) Innate immunity promotes tumor spread via myeloid cell mediated CD8+ T cell inhibition  D) Innate immunity promotes tumor spread via angiogenesis upregulation  E) All of the above 2) Which of the following is not a function of Macrophages?

 A) Phagocytosis and presentation of microbes or tumor- associated antigens to T-cells  B) Upregulation of acute phase protein production and systemic inflammatory response  C) Extrude a web of fibers composed of and serine proteases that trap and kill microbes extracellularly  D) Promote wound through increased angiogenesis  E) All of the above are functions 3) Complement cascade can be activated by the lectin pathway and the alternative pathway?

 A) True  B) False 4) Tumor associated macrophages are mostly M2- polarized, which is desirable for tumor eradication?

 A) True  B) False 5)Tumor infiltrating neutrophils promote tumor cell invasion and metastasis via matrix metalloproteinases ?

 A) True  B) False