𝐴2 𝒄𝒉𝒂𝒏𝒏𝒆𝒍

اي شي جديد ينزل بالقناة راح ينضاف لهذي الرسالة علمود الهوسة ف اذا احتاجيتوا شي مباشرةً شوفوه هنانه

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اي شي جديد ينزل بالقناة راح ينضاف لهذي الرسالة علمود الهوسة ف اذا احتاجيتوا شي مباشرةً روحوا للرسالة

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اي شي جديد ينزل بالقناة راح ينضاف لهذي الرسالة ف علمود الهوسة اذا احتاجيتوا شي مباشرةً روحوا للرسالة

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وصلتني هذي الملاحظات على ال immune response و ال transplantation يفيدون 👏🏻💯👆🏻👆🏻

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▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️ 🔴Parasitic infection: 📌 Helminth 📍IgE —-> eosinophilia + mast cell + TH2 📍TH2 تتفعل من خلال ——> IL25+33. …. TSLP( thymic …..) 📌 Both mucosal + tissue immune response By… TH2 📌 Protozoal : HIR+ CMIR Immune response may be Down or Up regulated خلصت🫠🫠🫠🫠🫠

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🔷ملاحظات عن Immune Response🔷 📌PRR of innate immune cell bind to PAMP of pathogen by 2 class of receptors: ▫️ NOD+TLR(3,7,9) ——> recognize microbes within cells ▫️C type lectin receptors ( Dectin + TLR1,2,4,5,6) —> recognize microbes outside the cell 📌 CD4 differentiated : ▫️TH1…( IL2 , IL12, IFNy ,TNF) —activate CD8, macrophage ▫️TH2… ( IL4, IL5) ——> B-lymphocytes to plasma cell 📌 CMIR ——> for intracellular microbes 📌 HIR——> for extracellular microbes 🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹🔹 🔴Viral infection: 📌 Innate immune: ▫️ IgA —> block viral attachment to mucosal epithelial cell ▫️cells of innate recognize Virus by … TLR ▫️ dsRNA virus—> produce ( IFNa + IFN B) resist replication + activate JAK- STAT—> transcription of genes ▫️ 2,5 oligo adenylate synthetase—> activate (RNAaseL) … degrades viral mRNA ▫️ dsRNA dependent PKR—> inactivate IF2 — block viral replication ▫️ IFNa+ IFNB —> bind to NK induces lytic activity ▫️ IL12 —> enhance activity of NK 📌 Adaptive immune: 🖇️Antibodies—> viral in blood ▫️ IgA bind to epitopes—> opsonize viral —> activate complement by C3b enhance Phagocytosis—> lysis viral by ADCC 🖇️ CMIR —> CTL against Viral Infection ▫️ APC present Viral by MHCll to CD4 produce : 📍 IFNy = increase expression of MHC class I, II 📍IL2= indirectly recruitment CD8+ macrophage 📍TNF= induce apoptosis ▫️ Viral infected cell present Ag by MHC l to CD8 … apoptosis by : 📍Exocytosis of granules content = create pores 📍 Cytokines = IFNy+TNFa+TNFB induce apoptosis 📍 CTL express (Fas ligand) 🖇️CTL most effector cells in CMI مهم 🔴 Virus can evade IR: 📍 inhibiting PKR= HCV 📍inhibit Ag presentation to CTL : a) inhibit Ag processing = empty MHC l = HSV b) down regulation MHC l = CMV+ adenovirus 📍 inhibit Ag presentation to CD4 = reduce level of MHCll = HIV+ CMV+ measles 📍inhibit Complement pathway: by proteins 🔹 bind to C3b= HSV 🔹bind to C4b= Vaccinia virus 📍 change Ag = influenza 📍 generlized immune suppression: 🔹destruction immune cell= HIV 🔹 produce proteins similar to human cytokine = EBV ( IL10) ▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️ 🔴Bacterial infection: 📌 innate = IgA —> PAMP recognize bacteria by TLR 📌 Adaptive: 🔴immune response to Extracellular bacteria: ▫️HIR= main protective response ▫️APC present Ag to CD4= TH2= produce IL4+5 = plasma c ▫️ HIR removal of Bacteria —> phagocytosis by C3b or Lysis by production (C3a, C4a, C5a) or lysis MAC ▫️ HIR inactivation of B.Toxin : 📍Exotoxin —> neutralizing Abs 📍Endotoxin—> LPS of (G-) activate complement & lysis 🔴immune response to Intracellular Bacteria : 📌 CMIR ——> delayed type 4 hypersensitivity // APC present Ag to CD4 —> TH1 —> IL2+ TNFy activate macrophage —> kill bacteria 🖇️Exotoxin = enterotoxin + exfoliating + TSST ——> act a Superantigen activate T-cell = excessive Cytokines= disease 🖇️Endotoxin( B.cell wall) = stimulate Macrophages = overproduction of IL1+ TNF—> cause Septic Shock 🖇️ Intracellular B. ( MT) = Chronic stimulation of CD4—> ⬆️ Cytokines ⬆️ activation of Macrophages——> giant cell —> granuloma formation 🔴 Bacteria Evade Immune: 📍For IgA= protease 📍For Phagocytosis = Capsule + M.protein + fibrin coat 📍For Surviving within phagocytic cell = ❌phagolysosome 📍For Ab = elastase = ❌of C3a+ C5a + hyaluronidase ▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️ 🔴 Fungal infection : 📌 cause Superficial + Systemic Infection 📌Growth of Commensal fungi in skin + mucous membranes Is Limited By Release of antimicrobial Peptides مهم 📌Innate immune : 📍Dectin 1 is CLR —> act PRR to recognize B 1,3 glucan 📍TLR—> 2,4,6= extracellular rec. —> GXM Mannan of fungal ……… TLR( 3,7,9) = Intracellular rec. —> DNA+RNA 📍Secretion of Cytokines ( IL2+4+6+10+12 … TNFa…TGFb) + Ros = present fungal Ag = elimination 📌 Adaptive immune: 📍IL6+TGFb= CD4——> TH17 = IL17 A+F…… IL22 📍IL12= CD4—-> TH1= release IFNy …… CD8+ macroph 📍 IL4= CD4—-> TH2 …… produce Ab 🛑 TH1+ 17 Most important T-cell for Fungal infection 🛑TH2 mediate fungal asthma + hypersensitivity

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🔹ملاحظات عن Transplantation 🔹 📌life saving treatments for cancer, organ failure,,,,,, 📌HLA= Strongest immunological barrier to allogenic organ + HCTs 📌HLA protein = target of response to Transplantation 📌 HIR+CIMR= both contribute in allogenic IR+ graft reject. 🔴MHC: ▫️class l= HLA- ( A+ B+ C) ▫️class ll = HLA- D ( R+ Q+P) 🔴Minor ( mHAs) ——> derived from normal cellular proteins ▫️exhibit variation in their amino acid sequence between individual——> lead to recognition as foreign by immune sys. ▫️Slower rate of rejection by ……… mHAs ▫️CD4+ CD8= recognize variations in MHC = rejection 🔴ABO : lead to very rapid rejection of Transplanted organs 🔴KIR+ MICA= target for allograft immune response 🔔 Allorecognition مهم 📍Autografts = same individual from one area to another like ( skin+ bone+ hair) 📍Allograft = between 2 genetically disparate individuals same species ( heart + lung+ liver) 📍Xenograft = between 2 individuals of different species like ( monkey to man) 📍Isograft ( syngeneic) between individuals genetically identical same species like ( identical twins) 🔴 Recognition of Alloantigens : 📍Direct = Recipient T- cell bind directly to foreign HLA on donor …… foreign HLA mimic self HLA 📣 Direct allorecognition ——> CD8 مهم 📍 Indirect = immune system reconize foreign HLA …… involve uptake + processing + presentation of foreignHLA by recipient APCs 📍indirect ——> induction alloantibody + chronic rejection 📣 indirect = CD4+ MO —> by cytokines —> DTH 🔴 Direct alloantigen —> recipients CD4 or CD8 direct recognize donor class ll or l MHC ——> differentiate to TH or CT = kill graft tissue cells 🔴 indirect alloantigen—> recipients APC take allogeneic MHC from graft tissue 🔵 Activation of alloreactive T cell : 📍 direct = donor dendritic cell in allograft migrate to Secondary lymphoid tissue—> direct present MHC to host T cell —— CD8 ( MHC l) —— CD4 ( MHC ll ) 📍 indirect = recipient dendritic cell in allograft transport donor MHC to SLT and presented to alloreactive host T-cell ( CD4) …… CD8 less important …… 🔹 CD8 = direct recognition MHC l 🔹CD4 = direct or indirect recognize MHC ll ▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️▫️ 🔴Hyperacute Rejection = min to hours 📍 mediated by preformed Ab 📍ABO+ HLA+ endothelial Ag ——> elicit HAR 📍 cause by blood transfusion , prior transplantation or exposure pregnant woman to feral Ag 📍Ag-Ab —> activate Complement—> thrombus —> ischemia & necrosis of transplant tissue 🔴Acute Rejection = Days to months 📍mediated by cellular alloresponse or Ab 📍ACR characterized by parenchymal + vascular injury— infiltration of CD8+ CD4 + MO ▫️CD8= cytotoxic reaction to foreign MHC ▫️CD4= produce Cytokines & induce DTH reaction 📍 diagnostic criteria: 1) deposition C4d in peritubular capillaries. 2) detection donor specific HLA ab 🔴Chronic rejection: graft atherosclerosis— fibrosis, scarring and narrowing lumen of vessel —— by proliferation of smooth M. 📍loss of graft First year post transplants 📍Factors induce CR // prolonged cold ischemia ,,,, reperfusion injury ,,, AR ,,,, toxicity from immune ⬇️ drugs 📍CD4+ B.cell+ Cytokines + Growth factor + IFN y + alloantibody ——> all lead to Chronic Rejection 🔴GVHD = HCT+ less common liver , lung —- lymphoid cell in graft mediate immune response against host HCAg 📍infused products contain mature T-cell benefits of this cells : 1) reconstitution of immunity 2) mediate Graft versus Leukemia effect 3) mediate GVHD 📌Acute GVHD= first 100 days post- infusion( skin+git+liver) 📌in mismatched stem cell trans.= target mismatch HLA 📌in matched S.c transplant = target mHAs 📍HLA phenotype = Complement dependent cytotoxic test 📍HLA genotype = use PCR- based amplification of HLA 🛑Screening + identification of preformed HLA ab —> incubation patient serum+ Lymphocytes with known HLA ag 🛑Crossmatching ——> Recipient serum + donor lymphocytes to confirm the absence of donor specific Ab

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اللي نزل بالقناة لحد هسه 👆🏻

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