L20-L25 notes for final.docx

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Microbiology and Immunology
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Microbiology and Immunology 3300B
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L20: Immunity to Infectious Diseases: p. 9.29-9.31, 13.1-13.6  Humans+pathogens co-evolved: successfully(JC virus) vs. no co-evoution(ebola) o JC virus: infected 90% of humans; initial infection in GI+mostly asymptomatic; stays forever w/o symptoms and pathology seen only in immunosuppressed ppl - only found it existed in HIV ppl o Ebola: infection rare, lethal(50-100% mortality); person-person transmission rare(only cause it kills you so fast otherwise it is highly infective); persistant/latent infections don’t occur  Virus wouldn’t want to kill host because that means it dies too  Ppl evolved w/ viruses: ex: malaria: plasmodiam showed up at same time, O blood type was protective ie. direct evolution due to virus – long evolution vs. quick evolution for protection against HIV in certain family in Nairobi: o 2 protective MHCs: HLA-A2 6802HLA-DRB1*01) – very fast: HIV came to humans from monkeys in 1931(HIV-1) and 1940+45(HIV-2A+B), last case in this fam was 1959  balance b/w host+path: host:min loss of fitnessselect successful MHC haplotypes, res genes+less-virulent path strain path: max repro successhost survival at least until transmitted elsewhere, avoid immunity, modulation of virulence)  Host pathogen interaction: pathogen must: survive in inhospitable human body(pH, temp etc); avoid/mod immune response to allow own survival :. Most microorganisms not pathogens+have immune-avoiding mech Avoid innate: 1) prevent opson 2) shut down TLRs 3) prevent GPCR 4) disrupt phagocyt 5) killing immune cells 1. avoid opsonizationavoid C’, Ab binding:. Phagocytosis – good survival mech for EC pathogens  ex: lyme disease(borellia): coat surface w/ factor H=inhibit C’ deposits by exotoxin(CspA) binding facH  ex: syphilis(treponema): coat surface w/ host proteins to hide Ag/cell surface from Ab+C’ o syphilia “sticky” :. non-specific binding to charged lipids in bac mem, hides own Ag  ex: streptococcus: more complex; directly interferes w/ Ab by 2 toxins (proteins A+G) bind to IgG via Fc domain(part of Ab that activates C’+binds FcR) :.even if Ab bound to bac, toxin blocks part needed for phagocytosis+C’ activation 2. ex: Brucella(pneumonia) and UTI(e. coli): avoid being seen by shutting down TLR; have exotoxins(TcpB+C) which bind TIR of TLR(TIR bind Myd88; 1 step in signaling) 3. pertussis(whooping cough): chem mod Ga to prevent GDP/GTP exchange:. Cant turn on GPCR/chemokines recruitment cascade for WBC rolling/adhesion/diapdesis needs chemokines:. Prevent WBC leaving blood to ineffected tissue and for chemotaxis to site of damage; ox burst also signals w/ fMLP+GPCRs 4. some bac live in phagosomes; have catalase to convert H O2H2O; 2an block lysosome/granule fusion(TB+leprosy) or change phagosome mem to make it look like normal cell(lipid makeup to look like mt/ER etc ex: chlamydia) 5. ex: streptococ+pseudomonas: pore-forming toxins(hemo/leukolysins) lyse leukocytes(sometimes specific fxnlisteria Case Study I: Listeria  food poisoning, wont die in fridge+grows, very serious since ppl get large dose since it always grows  2 toxins(INIA/B): med adhesion+invasion through gut vili via cell extrusion; adhere to TJ proteins reorganize to extrude epithelial cellpost-internalize access lymphaticsMΦ main target+induce own phagocytosis - adhesion+ MΦ invasion by toxins+PRRs phagosome lysis by LLO cell-to-cell spread by expressing ActA to polymerize actin s.t whenever it crawls+bounces against wall it causes mem extensions:. - MΦ knows its being attacked+if noninfected MΦ poked it tries to ingest that object ie. other MΦ ;. Ingests small piece of 1 phagosomelisteria spreads very efficiently - Immunoavoidance: avoid C’+Ab, escape phagosomes, inhibit MΦ through PLC, hemolysins(diff purpose from cell lysis), proteases –make MΦs less bactericidal,  early immune response: IC pathogens activate cytokine(CCL2) response via NODsactivate monocytes+DCsTNF, INFy, NO from active cells induce death of infected cell -in advanced infection PAMPs/DAMPs can leak out and activate TLRs and more immune system cells come on  overall apoptosis  adaptive immune response: 2 routes to clear listeria: 1) presentation by classical MHC I path 2) presentation by nonclassical(MHC-Ib) by formyl-peptide specific H2-M3 –look for bac specific transcripts into MHC+present to CD8 overall induce apoptosis of infected MΦ w/ MHC I+H2M3 Avoiding adaptive immunity: 1) antigenic(genetic) variation 2) antigen shift+drift 3) immune privilege+latency **EC paths** 1. 1000s of pneumonia strains that all vary based on surface protein :. Cant use memory against it 2. drift(point mutation, some residual imm)+shift(large changes ie. gene swap, no residual, severe pandemics) o ex: flu: H and N Ag on surface(naming flu: ex: H1N1) and each Ag on diff chromosome o ex drift: neutralizing Ab against hemaglutinin block binding to cellsmutation alter epitope in protein s.t neutralizing Ab doesn’t bind accumulate point mutation in H or N allele+Ab ineffective  flu vaccine just to hold it in check until immune system catches up – ie. less mild, residual imm o ex shift: RNA segments exchanged b/w viral strains in 2 host :. No cross protective immunity to virus w/ new hemagglutinin if 2 flus infect same cell don’t know which chr in proper virus when being packaged very bad since no Ab against new H or N  antigenic shift via gene conversion: 100s copies of gene all slightly diff and similar to vdj recomb pathogens pick a copy, translocate to site w/ DNA sequences to make protein then make Agrepeated infections because of gene changes  ex: protozoans(sleeping sickness, malaria) o ex: many inactive trypanosome VSG genes but only 1 site for expressioninactive genes copied to expression site by gene conversionmany rounds of conversion:.allow trypanosome to vary VSG expressed 3. privilege(min/no imm accessex: herpes) or latency(min path activity, few/no Ag madeex: mononucleosis(Epstein-barr virus) – note that when mono reactivates it can give you cancer 4. immune modulation : viral strategies include inhibiting humoral or inflame response, block Ag processing+presentation, immunosuppression of host mech: virally encode Fc/C’/chemo or cyto kine, cytokine receptors/homologues, inhibit adhesion molecule expression, mimic TLRs, inhibit MHC I/TAP etc, IL-10 homolog Case Study II: Leprosy: a “genetic” disorder  infective: mycobacterium leprae, can treat w/ antibiotics, damage due to infection of MΦs, epithelium+nerves by path eating cartilage/bone  genetic: only ~5% ppl susceptible, need specific allele:. inheritable o susceptibility genes involved w/: PRRs, C’, TAP cytokine, MHCII molecules, co-stim, HSP, etc o mutations det how infection proceeds: 2 ways: develop either Th1 or Th2-med  th1: HLA-DR2/3, others(not bad response, ppl don’t suffer much) OR Th2: HLA-DQ1, other  Th1: monocytes recruited to infected sitesdiff to MΦ +DCDCs have non-classical MHC CD1b+(sim to fMET- presenting MHC but present leprosy lipoproteins to CD8release INFy tells MΦ(w/ CD16+FcR) to make ROS+protease  Th2: bad; monocytes don’t turn into DCs w/ specialized MHC for leprosy; have nonclassical MHC to present other Ags (unknown mech, other DC sources etc) good at making B cells but Ab in response to path living in cells isn’t good way to kill it since Ab outside cell also since activate CD4+Th2=no MΦ activation and MΦ s are great at killing pathogens Tuberculoid leprosy (Th1) Lepromatous leprosy (Th2) Organisms present at low to undetectable lvls Organisms show florid growth in MΦ s Low infectivity High infectivity Granulomas+local inflammation: Disseminated infection: peripheral nerve damage bone, cartilage+diffuse nerve damage Normal serum Ig levels Hypergammaglobulinemia - don’t need Ab response for Th1,no unusual lvl - extra Ab but useless since bac living inside cells Normal T-cell response: specific to M. leprae AgLow/absent T-cell response: no reponse to M. leprae Ag - leprosy specific CD4+CD8 - poor CD8 and only see Th2 CD4 types  Granuloma: infected cells w/ surrounding immune cells to prevent infection spread Review slide:  To be infective, much have mech to overcome immune system  hide pathogen elements, alter system to ones less able to clear pathogen  even with those virulence factors immune system can usually clear/control path L21: Immunological Tolerance: sec 15.1-15.7, 12.15-12.20  Tolerance: non-responsiveness to Ag  self-tol(non-responseiveness to self) vs.acquired(induced) o Acquired: suppress specific, systemic immune response to forein Ag induced by specific action of lymphocytes  Fetal-tol: in developing fetus OR oral-tol: suppression against Ag encounted via enteric(oral) route Layers of self-tol: Type of tolerance Mechanism Site of action Central tol Deletion, editing Thymus, bone marrow Ag segregation Physical barrier to self-Ag access to lymphoid systemPeripheral organs(ex: thyroid, pancreas) Peripheral anergy Cellular inactivation by weak signaling w/o costim 2 lymphoid tissue 0 Reg T cells Suppression by cytokines, intercellular signals 2 lymphoid tissue+sites of inflam Fxnal deviation Diff of reg T cells that limit inflame cytokine secre2 lymphoid tissue+sites of inflam Activatin-induced cell death Apoptosis 2 lymphoid tissue+sites of inflam  Most mech shared b/w self_induced except for central tol(no role in mediating tol to foreign Ag) Ag segregation: most self-Ag retained outside lymphoid system by physical barriers(cell mem, endothelium etc)  In absence of tissue damage these Ag not encountered by immune cells (since they stay inside cell not EC)  Privileged sites: brain, eyes, testes, placenta, fetus: similar to Ag-segregation; immune system excluded from sites o Discovered by grafts into these tissues surviving w/o immunosuppressants since sites can tol intro of Ag w/o eliciting damaging immune response  7 mechanisms 1. restricted entry of immune cells: BBB has tight epithelial cells 2. expression of MHC Ib instead of classical MHC I: don’t present proteins, instead fMET, LPS etc ie. not self-Ag 3. high expression of C’ inhibitors: C’ major in opsonizing/drives lysis:.suppress other activities, particularly phag 4. local production of TGFb: and other immunosuppressive cytokines; basal expression here to inhibit immune cells in area and important role to drive lymphocyte subsets to suppress immune response in those areas 5. minimal/no draining lymphatics: no way for Ag to even get to lymph nodes+be presented 6. const expression of apoptosis-including ligands(FASL, TRAIL): induce death of any immune cell trying to enter 7. tissue-specific immunomod  placenta: expression of indolamine 2,3-dioxygenase(IDO) remove tryp :. Prevent T-cells proliferating – since they cant grow w/o getting tryp from environment  FAS/FASL system: allows immune-privileged tissue kill incoming immune cells o Immune cells have FAS(receptor)FASL trimer binds FAScluster death domains(DD)recruit FADD via DDs clustered death effector domains(DED) recruit caspase8 which starts off apoptosis cascade Case Study I: Placental/fetal immune privilege:  50% of fetus’ proteome is foreign ie. some Ag wont have any close match in maternal genomemale child has 12+genes w/ no homologs/paralogs in mom –also MHC haplotype is diff so rejection similar to transplanted tissue  3 layers of cells b/w moms immune system+fetus but fetal syncytiotrophoblast in direct contact w/ mom blood  placenta = immunological barrier physically(limit by synctitia-fused cells w/o junctions) and immune barriers o immune barriers: no HLA-A/B/C expression and have HLA-E+G instead(minimally polymorphic, interact mainly w/ NK cells) also many mom Tregs, neurokinin B(suppress T cell activity), IDO(breakdown tryp) and phocphocholine(suppress T cell) suppress immune response enzymatically, high expression of FASL  problem for fetus is doesn’t have adaptive system(doesn’t begin until after birth) :. High risk of infection o transport Ab from mom via FcRn on syncytiatrophoblast can grab Ab from mom blood and dump into fetal blood ie. this is passive immunization AND moms milk secretes Ab and same FcRn can pick them up from infant gut and release into circ 2 mechanisms of mom giving fetus+newborn adaptive response  rhesus(Rh) disease: maternal Ab gone wrong: if mom is Rh- and dad is Rh+ chance of baby being Rh+ is fine until mom has 2 child cause then she developed anti-Rh+ Ab from blood mixing during birth :. Now baby gets disease o C’-med lysis of RBC:. Fetus anemicdep on quantity of Ab produced can lead to low birth weight or death o Prevention: Rh- moms injected w/ purified anti-Rh IgG soon after birth of Rh+ child :. Any Rh+ cells which transfer to mom during birth destroyed before immune response induced Peripheral tol(anergy)  series of processes which prevent immune response in peripheral tissues  3 mechanisms: Ag concentration, induced anergy(probs most important) and removed of GC B-cells  [low Ag]= ignorance: insufficient Ag to activate TCR/BCR but can later activate w/ co-stim  [high Ag] = saturate all BCR:. Cant crosslink:. Doesn’t activate cell but strong stim of BCR/TCR can induce apoptosis activation-induced cell death (AICD): repeated exposure to same Ag in periphery induces upreg of FAS/FASL in T cell o Pathogenic Ag usually rare:. Encountered occasionally, self-Ag common so serial encounters common o FAS/FASL expression sensitizes T-cells to apoptosis limitation in developing anti-cancer vaccines  Induced anergy: some DCs present Ag w/ only activation signal(no costim):. T cell apoptosis or inactivates(anergy) o In anergy 2 proteins(GRAIL+Cbl) upreg’d locking TCR into inactive state  Removal via SHM+T :regpermutation: bypasses central tol+helper-cell med activation:. Can form auto-reactive B cells but removal due to [expected Ag] in GC acts as signal to kill itself  Reg T-cells: naturally derived from weakly self-reactive T-cells in thymus vs. induced derived from T-cells encountering Ag in presence of co-stim+cytokine signals(TGFb)express CD4 CD25 FoxP3 +make IL-10+TGFb o Natural Treg weren’t killed by central tol; overall natural+induced are the same just from diff places  Review of peripheral tol: - Ag conc: low=no stim of TCR/BCR vs high: saturation of TCR/BCR and/or AICD - AICD: repeated encounters w/ Ag, upreg FASsensitize immune cells to apoptosis - Induced anergy: when Ag encountered w/o costim/helpanergic cells have min replicative ability+cant engage in effector responses - Treg: weakly self-reactive, inhibit adaptive immunity via cytokines(TGFb + IL-10) Oral tolerance : mechanism to let us eat food  vs. protective won’t let us Protective immunity Mucosal(oral) tolerance A0tigen Invasive bac, viruses, toxins Food proteins Commensal bac 1 Ig produced Intestinal IgA, specific Ab in serumSome local IgA, low/no Ab in serum Local IgA, no Ab in serum 1 T-cell response Local+systemic effector + memory No local effector No local effector Response to re-exposure Enhanced (memory) response Low/no response Low/no mucosal or systemic  Induce by: [Ag], induced Treg, induce anergy/specific apoptosis in Ag-specific T-cells, high basal TGFb+IL-10 in GALT o Experiment: feed mouse ovalbumin(in chicken eggs, mice don’t usually encounter it) or control day 7 inject w/ ovalbumin+adjuvant to stim effective immune responseie got protein by 2 diff routes results show no immunological consequence after subQ injection even if Ag got through in way normally associated w/ response vs. control show regular response Case Study II: Gut Flora  Don’t want a response since they help digest food+fight off bac BUT have same PAMPs so how to deal w/ them  Gut mucus in 2 layers: inner(large [mucus glycoproteins, IgA, antimicrobials] and outer(chem diff, portion digested)  Gut flora don’t go into inner layer:. Don’t see PAMPs/Ag:. TLRs there don’t react since bac in gut lumen/outer layer o Exception: M cells take intact bac from gut lumen/mucus+transport across to peyers patches+isolated lymph follicles important to maintail tol since transport gut flora in way that’s not immunostim(instead passive for bac=no PAMPs released:. No infected cells having receptor-indep activation)  Normal response: Ag presentation in peyer’s patches: absence of danger signals/other invasion signs(ie. activate NODs)  in presence of commensal bac, production of PGF, TGFb and TSLP inhibit DC maturationin mesenteric lymph node immature DC secretes IL10+RA + has weak costim+TCR activation to induce differentiation into T-reg + o Drive IgA class-switch in B-cells, low-grade “phys” inflammation+diff to T-reg or anergy in flora-specific CD4 T - Pathogen response: interact diff w/ gut epithelium(adhere, damage barrier, IC path of epi cells/underlying immune structural cells  allow PAMPs across epithelium, induce release of DAMPs from damaged cells, activate IC PRRs(NODs, TLRs, invade phagocytes also)activate DCs to diff to Th1/2/17 - DC has lots co-stim+TCR activation(B7/CD28, CD40/CD40L, secretes IL-12) flora-human co-evolution: path recognition by TLRsinitiate cascade of signals activating IKK(NFkb/Ikb interact)IKK phos’s Ikb targeting it for degradation:. NFkB translocates to nucleus to activate txn - some commensal bac block txn by activating PPARy to prevent NFk from binding target promoters:. Causes its exportation from nucleus or some block degradation of phos’d Ikb:. By not releasing NFkB prevents it translocating - basically how gut flora w/ same PAMPs use chemicals to modulate activity L22: Cancer Immunology: 16.13-16.18,  2 mechanisms of immune system to cause cancer: 1) chronic inflam risk at that site 2) ROS/RON mutate DNA o ex of chronic inflam: IBD10% ppl develop colon/rectal cancer vs. general pop only 0.05% develop it o ex: helicobacter pylori: chronic stomach ulcers  some viruses have cancer-causing genes(oncovirus, Epstein-barr virus lives in B cells, causes mono+possibly cancers in B cells, Kaposi’s sarcoma virus found in HIV, human papilloma virus ie. HPV)  infections may cause up to 25% of all cancers and vaccination against these viruses can prevent these cancers Case study I: human papilloma virus (HPV) vaccine  cervical cancer is 5 most common cancer in women; incidence 16/100,000women, ~250,000 deaths per year o death rate doesn’t consider other cancer types(only cervical) :. Actually underestimate  HPV serotypes(strains) 16,18,6,11 cause 90% of all cervical cancers – also anal, vaginal, penile, head, neck, oral o 16+18 mostly; 6+11 cause warts then cancers in certain circumstances  HPV vaccine: guardacil(protect against 16,18,6,11), cervarix(protect against 16+18)both are “empty”(no genome) virus-like particles w/ HPV proteins ie. capsid or whatnot :. Not infective or reproducing o Hard to see if it works because cancer takes years to develop, but can look at early signs of cancers such as persistant infection w/ 16+18 serotypes+pre-cancer lesions o Vaccinated compared to control had 80% protection and w/ lesions protection seems 100% o Note: table in notes looked at intraepithelial neoplasia(CIN2+) or adenocarcinoma in situ(AIS) due to HP Inflammation and Tumor Progression  Tumors are chronically inflamed and inflammation has 2 purposes: o 1) angiogenesis gives tumor w/ blood/nutrients 2) creates microenvironment which suppresses Th1 response  angiogenesis: needed for growth(transport O 2nutrients); tumors make growth factors(VEGF) and if the 1-2mm tumor doesn’t make new vessels it will stop growing; blood supply also give tumor access into circ for metastasis o angiogenesis needs immune cells which “cut a channel” b/w immune cells and it makes pro-angiogenic factors s.t endothelial cells start crawling into channel to make new blood vessels o n-phils drive angiogenesis: experiment: depleting w/ Gr-1 reduced availability of pro-anngiogenic factor VEGF  tumor-associated macrophages: M2, alternatively activatedsecrete anti-inflam+prohealing IL-10, TGFb, , nphil attracting(CXCL1,2,3,8, VEGF, VEGA) vs. norm/inflam/phagocytic M1 TNFa, INFy, IL-12, ROS/RNS/proteases o start as monocyteenter tumor+encounter cytokines to differentiate into M2(M-CSF, IL-4/10/13) M2 recruits n-phils+promote angiogenesis(CXCL1,2,3,8, VEGF, VEGA)nphils promote angiogenesis(VEGF, chemo/cytokiens) also make IL-10+TGFb to promote more M2+go towards Th2+Treg which suppress cancer fighting  lastly M2 makes growth factors+tissue repair proteins to help tumor heal+grow+stop apoptosis  inflammation can kill cancer: ROS, RNS, proteases, pore-forming proteins, antibody-dep cell cytotoxicitiY(ADCC) inflammation+cancer summary:  few chemokineslimited inflammationrestricted vascularizationrestricted tumor growth – SLIGHT growth  abundant pro-inflam chemokinesinflammationneovascularization RAPID growth  altered balance of pro+anti-inflam chemokinesxs inflammationangiogenesisiontumor REGRESSION/DEATH adaptive immunity and cancer:  first experimental evidence: mice w/ certain immune mutations(yd T-cell deficient, RAG/STAT1 or perforin knockouts) have higher incidences of cancer note: RAG=no T+B, STAT1=signaler for mature T, perforin=kill w/ CD8) o immunize mouse w/ irradiated tumor cellsinject viable cells of same or diff tumorresponse to irradiated wont elim unrelated tumors of diff cell while response to unique tumor rejection Ag does:.Ag-dep response  hypothetically tumor Ag should show tol since its just a human cell but extra growthhow to get tumor Ag: o mutations: create aa substitutionsnew Ag o Ag found in immune-privileged sitesmost commonly testes Ag in breast cancer; also in men but basically the immune system never got a chance to show tol to it since never saw it in the site before o Developmental Ag: self proteins that immune sys wont encounter since no adaptive in fetus o Overexpression; unusual post-tln mod, viral oncogene; chr rearrangement/recomb  Immunosurveillance: process of adaptive system looking for cancer cells/tumor Ag/other signscan downreg MHC I, use NK for recognition in theory find every tumor+kill it before it grows and if not to cancer immunoediting:  Immunoediting: immune system drives tumor evolution to get around surveillance; tumor cells mutate a lot causing heterogeneous cell mixture so if mutation lets cancer avoid immune it grows betternew cells accumulate more mutations and over time becomes different enough for immune system to recognize it as foreign  3 phases: elim phase(surveillance: tumor arise in tissueimmune cells recognize+eliminate)  if fail go to eq phase where variant tumor cells arise that’re more res to killing by NK+CD8) and over time variety of diff variants develop escape phase(eventually 1 variant escapes killing mech or recruit reg cells to protect it:.spread unchallenged tumors avoid immune system: 5 mechanisms 1. low immunogenicity: no peptide:MHC ligand, no adhesion molcules or co-stim molecules (hide MHC/other recognition ways but then missing MHC = target for NK so instead of downreg MHC, downreg costim/adhesion like CD28, LFA1) 2. tumor treated as self-Ag: tumor Ag taken up+presented by APCs in absence of costim to tolerize T-cells 3. Ag modulation: Ab against tumor surface-Ag can induce endocytosis(destroys Ag) this also prevents C’ and helps remove the Ag from surface:. Prevent addition Ab binding=immune selection of Ag-less variants 4. Tumor-induced immune suppression: tumor cells secrete factors(TGFb, IL-10, IDO) to directly inhibit T +induce T-reg 5. Tumor-induced privileged site: secreted factors create physical barrier to immune system Targeting cancer w/ adaptive immunity:  Immunotoxins+ADEPT: take Ab directed against tumor-Agattach to toxin(bac toxin=immunotoxin) or chemo drug/radiation source(Ab-directed enzyme/produg therapy =ADEPT)  either way selectively delivering something poisonous to cnacer cell = treating the cancer and not entire body  Hairy-cell leukemia: BL22 immunotoxin: Used anti-CD22 Fv(where Vf / just the Fab portion, linker + exotoxin(PE38) bind CD22 found against mature B cells(particularly hair-cell leukemia)2/3 ppl showed complete remission after this therapy -CD22 = mature B cell surface marker; PE38(pseudomonas exotoxin; one of most potent known toxins) Case Study II: Sipuleucel-T: a prostrate cancer “vaccine”  Prostrate: 2 leading cause of cancer deaths in US men(#1=lung); probably most common in males(80% by age80) o Mostly slow growing w/ 15% malignant and rapidly growing  Current treatment of aggressive form: castration(most metastatic protrate tumors are androgen-sens; only temp benefithormone refractory prostrate cancer(HRPC) comes back in like 2 yrs since doesn’t need hormone o Docetaxel chemo targets HRPC; and overall cancer drugs are harsh and shorten your life more than cancer  Sipuleucel-T: approved in april 2010, take blood+isolate immature DCs(leukapheresis iDC)combine prostratic acid phosphatase ie. prostrate cancer specific Ag) and GM-CSF growth factor lets DCs maturereinject mature DC that is now Ag-loaded mDC and presents the prostrate-Ag in a way to activate Th1 response  DC cell vaccine h
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