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LO1: desc cellul and humoral compons innate and adap imm sys.

-1st barriers to hum infec- epith not effec alone.
Physic imm sys facil clearance pathog from epith- rap regen, blinking, tears, ear wax, nasal hair, cough, sneeze, microciliary escalator, vom, dig enzs, peristalsis, regul urine flow.
-epith prim role block microorg. Func in secs of pathog contact. Mech, selec perm Barr to outside. Prod nat AB-cat ionic AB peps-defending and catheliadins. Poss motile cilia. Rap renew. Prod cytokines-alt behav other cells. Prod chemokine- attr other cells to most conc pt Ie epith. May prod muc ins- goblet cells etc. Transp Ab inside to outside eg IgA gut to lumen.
-imm resp- pathog with non self Ag dams epith. Epith activ. Chemokine and cytok prod and diff to LP and BV.
-pathog to epith to activ epith to cytok to perm endoth to cell and fluid mig into CT (prot, imm cells) to opsonisation to phagoc to interac with other cells of innate and adap IS.
-vasc perm incr main by inflamm meds= incr fluid leak and extravasated of Ab and complem at infec site. Mig of Mac, neutroph, lymphoc to tiss also increases as does their microbe ideal activ.
Pain= protec and recover.
Heat/calor, swell/tumor, red/rubor, pain/dolor, LoF/functio laesa.
-see innate vs adap diag.
-metchnikoff 1893 cell med imm. Phagoc starfish. Phagoc mig quick to site infec or dam.
Ehrlich 1900 humoral imm Ab.
Wright 1900s factors ins serum incr phagoc-opsonisation.
Humoral and cell med act interac.


LO2: desc main diffs btw adap and innate.

-innate- inbuilt resp to resis infec. Non specif eg targs mannose/LPS. Not incr by second expos. No memory. Uses cellul and humoral compons. Reqs adap. Triggs and amplify adap.
-adap- est to adap to infec. Specif/acq. Incr by second expos. Memory. Uses cellul and humoral compons. Reqs innate. Ab refl infects been exposed to.


LO3 eg of coop and interdep of innate and adap imm.

-see diag.
-Mac- phagoc microbe or dam/unwanted cells. Rel var cytok imp in innate and adap. Mac long lived, gen lysis as req. profess APCs in dev adap imm, present to T. T contr adap resp, recog Ag presented on MHC by T/Mac/B. R med endoc of bact.
-opsonisation- coat microorg Ab/complem=recog as foreign by phagoc. Encapsulate bact not ent by neut. Ab bind bact activs complem and C3b bind to bact=effic eng by neut med by FcR and complem Rs. Grans fuse phagolysos rel tox O metabols kill bact.
-NK no classic Ag Rs- part innate. Recog and kill abn cells eg tumour. Direc induce apop in vir infec cells by pump protease through holes make in targ.
Sim to CTL but no specif TCR. Innate imm Ag intracell infec eg vir. Lack NK= persis vir infec esp herpes, not clea by norm adap resp. NED each other.
Mast cells prod IFN a and b if vir infec. And Mac prof IL12 and TNFa. Both cause NK activ and prolif.
NK prov early resp vir infec. Slower CTL resp devs to clear. (See diag)



-imp implied by rarity of in her defic in innate mechs. V impaired protec when do occ.
innate acts early- defic causes init v rap prolif microorg.
Adap slower- lack can contr but not get rid compl.

cells in innate:
-Mac/monoc in CT- biggest WBC. Phagoc. AP to lymphocs.
-Neutroph PMN- 5 lobe nuc. Phagoc. Anti bacterial. Gran cytop. Neut and basophil cytop grans bind E=red. Neut most numerous WBC, X chrom stick out in fem.
-Eosinophil- prob evolved as anti parasite. Allergy. Eg att schistosomes in presence IgE from infected pt- sec enz and inflamm meds etc. Give allerg resp inapp eg enz on pollen.
-Basophil- ?protec of mucosal surfs. Allergy. Grans. Basophil grans also bind H, can obscure nuc.
-Mast- in tiss, rel inflamm meds if surf Ig X link. Protec muc surfs. Allerg.
-phagocytes- Mac and neut active eng to phagosome and destr bact as lysis bind, EC vir and imm complexes.
-neutroph- not in healthy tiss norm. Each day 3x10^9 ent tiss of oral cav. Spec for work anaer conds that prevail in dam tiss. Neut arriv 1st resp event of inflamm resp- markers of acute inflamm. Can't synth new grans, dies once used. Defic=receurr infec commensalism flora eg S epidermidis. Somet phagoc rel lysis conts onto outside of pathog eg if too bid to dig. Eg in gut enz also prod diarr= wash out bact.
Bact bind neut Rs=phagoc and kill. Eg neut exp LPS R (CD14), mannose R, CR3+4, glycan R, scav R.
-secretory molecs of innate imm sys-
Transferrin and lactoferrin deprive microorg of Fe.
IFN inhib vir replic and activ other imm cells to kill.
Lysoz in serum and tears breakd pg wall of some gram pos but synergism with...
Antimic peps.
Fibronectin opsonizes bact=prom phagoc.
Complem compons and prods- destr microorg direc of help by phagoc cells.
TNFa supp vir replic and activ phagoc.
-complem sys- disc as heat labile compons that complem/incr ops on effs of Ab. Mark for destr by cov bind surf. Pre dates Ab evol. Ab resp evolved to enhance mechs of complem activ and phagoc.
Complem prots ubiq in blood and lymph. Can be used mimed on infec. Ab later enhance complem activ.
C1-9 complem casc. Cause rec inflamm cells, opsonisation marking, direc kill by MAC Pore. See diag.
Inher complem defic- C1/2/4 imm complex dis (T3) eg SLE. C3 can't mark phagoc=receurr bact infec (pneum, septicaemia, mening).C5/6/7/8/9 MAC miss less effs- receurr Neis infec only consis clinic prob, poss mening and gonorrhoea.



T and B resp to Ag=specif resp when intro to tiss. Comm lymphoid progenitor. T dev in thymus, B in BM.
T form Th which activ B and Mac, and CTL kill infec cells, v specif, tum and vir infec cells.
B form plasma=Ab. Big, lot ER, one specif Ab.
-lymphoc Ag Rs-
Lyc- lymphoc inactiv til encounter Ag. Exp Ag Rs.
B- AgR is mem bound Ab-surf Ig. B prod Ab-some bound some rel.
T- AgR NOT mem bound Ab, but distinct molec- TC AgR.
Each AgR binds specif Ag. Each cell 1 specif. Big repetoire. Clonal expansion on activ. TCR diag.
-3 main mechs Ab protec host-
Neut- Ab prev bact adherence eg gut bact cov IgA.
Opsonisation- Ab prom phagoc. R for Ig and complem.
Complem activ- Ab activs complement=enhance opson and loses some bact.
-clonal adap resp- each naive lymphoc with unique R is poten progenitor of genet identic clone of daughter cells.
BUT clonal distrib of AGRs mean lymphocs of 1 specif too infreq to=effec resp. Clonal selec incr clonal freq of cells with partic Ag specif.
-clonal selec theory- McFarlane 51.
Ag interac= lymphoc activ. Clonal selec induces prolif and incr effector cell freq. thresh protective effector func. Above=can clear. Slow adap resp.
-phases of adap resp- diag.
Recog, clonal selec and expansion, and diff to effector. Activat. Effector- Th and CTL, Ab prod effects. Humoral and cell med imm elim Ag. Decline- homeostasis, T and B apop. Mem seeding of mem T and B specif cells not decr to prev lev.
See mem diag.
-Th can't see foreign unless present by APC. B can't become plasma unless Th bind.


Links btw innate and adap-

Activat complem by Ab.
Adherens Ab to mast and Mac.
Th help Mac.
Cytok from Mac to T and B.
Mac present to T and B.
NK cytotox.



-pathogens= dis causing microorganism psych eg Protozoa,bact, vits, fungi, worms.
-prot roles- nutr acq, repro, locomot, resp. Pathogen prots diff to hum, allow surv in niche. Imm sys detec AA seq diffs.
-why dam host if alerts imm sys- need to break barriers to access env for colon.