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Path 6 Immuno
LECOM Path Ch 6 Immunology
| Question | Answer |
|---|---|
| Type I hypersensitivity Immune mechanism | Production of IgE-> crosslink on mast cell FcR-> releases histamine, enzymes, heparin |
| Type I hypersensitivity causes | edema, SM contraction, vasodilation, increased mucus; later recruits inflammatory cells |
| Prototypical Type 1 hypersensitivity reaction Disorder | Anaphylaxis; atopic bronchiole asthma |
| Lipid mediators released in Type I HSR | PAF, PGD2, LTB4, C4, D4 |
| Mast cell degranulation can be activated by | IgE, C5a, C3a, IL-8, temperature, adenosine, codeine/morphine |
| Type I HSR late phase consists of | eos, neuts, basos, monos, CD4+ T-cell infiltrates |
| This IL helps differentiate T-cell into TH2 cell | IL-4 |
| TH2 cells release these 3 IL’s, and their actions | IL-4: Induce B-cell IgE switch, and TH2 cell growth; IL-5: develop and activate eosinophils; IL-13: enhances IgE and mucus production |
| These are the two most potent vasoactive and spasmogenic agents known | LTC4 and LTD4 |
| This is the most abundant mmediator produced by mast cells | PGD2 |
| LTB4 does what? | chemotactic for neuts, eos, and monos |
| Most potent eosinophil activating cytokine known | IL-5 |
| Atopic individuals have increased what compared to normal people? | increased serum IgE levels and increased levels of IL-4 producing TH2 cells |
| Loci associated with atopic individuals | 5q31; IL-3,4,5,9,13, and GM-CSF |
| Type II HSR Immune Mechanism | Produce IgG or IgM-> bind cell surface Ag or tissue->target cell destruction by compliment or FcR |
| 5 Type II HSR Prototypical Disorders | Autoimmune hemolytic anemia, Goodpasture’s Syndrome, Acute Rheumatic Fever, Myasthenia gravis, Graves Disease |
| Type II HSR activates the compliments system by what pathway and produces what 2 byproducts, and what do they do? | Classic; C3b/C4b; deposit on cell surface, opsonizing the cell |
| IgG Ab on a cell causes and leads to what? | opsonization; phagocytosis |
| What is ADCC? | antibody dependent cellular cytotoxicity |
| Inflammation in Ab and Ab-complex HSR (II/III) is due to ____ and _____ | complement and Fc receptor dependent reactions |
| Type III HSR has a propensity to attack | vessel walls |
| 3 steps of Type III HSR are | formation of complex in circulation; deposition in tissue; inflammatory reaction |
| Formation of Ab-Ag complex usually takes | 1 week |
| The most pathogenic complexes are: what size? Formed with excess Ab or Ag? | medium sized and formed in slight Ag excess |
| Clinical Sxs of Type III HSR usually present how long after injection? And what are they? | 10 days; fever, urticarial, joint pain, lymphadenopathy, proteinuria |
| What can be measured to monitor the activity of Type III HSR diseases? | C3 levels; get used up during episodes |
| Morphology of Type III HSR: | acute necrotizing vasculitis; many neuts; “fibrinoid necrosis”; IF stain shows lumpy granular deposits of Ig and compliment |
| Localized area of necrosis on skin, immune complexes seen in vascular beds. Name of reaction? | Arthrus Reaction |
| Type IV HSR is mediated by which cells and after what? | CD4+ T-cells: environmental and self-antigens; CD8+ T-Cells: post viral infection |
| CD4+ T-cell HSR are also called what ? | DTH- Delayed Type Hypersensitivity |
| TH1 cells mediated disease is dominated by what cells? | Macrophages |
| TH17 cell mediated disease is dominated by what cells? | neutrophils |
| Upon recognizing Ag on APC’s CD4+ cells secrete what? And it does what? | IL-2: autocrine growth factor |
| What must APCs produce to induce TH1 cell differentiation? What also promotes TH1 cell growth? | IL-12; IFN-γ |
| What must APCs produce to induce TH17 cell differentiation? What also promotes TH17 cell growth? | IL-1, IL-6, IL-23; w/ TGF-β |
| TH1 cells mainly secrete what? | IFN-γ |
| What cell does IFN-γ affect in Type IV HSR? What does it do? | macrophages; altered to express more MHC-II |
| What do altered, activated macrophages in TH1 cell meditated Type IV HSR secrete? | TNF, IL-1, IL-12 |
| TH17 cells secrete mainly what? | IL-17, IL-21, IL-22 |
| What does IL-17 and IL-22 do in TH17 cell mediated Type IV HSR? | attract neutrophils and monocytes |
| What type of HSR is contact dermatitis? | Type IV |
| Morphologically, what is characteristically seen in DTH-SR? What type of cells, and where? | mononuclear (CD4+) and macrophages, perivascular cuffing; venules with endothelial hypertrophy |
| With chronic disease, what is seen after 2-3 weeks? What is the predominant cell? | granuloma; epitheliod cell , which is a transformed macrophage |
| Two preformed mediators involved in CD8+ cell mediated killing? | perforins and grannzymes |
| Mechanism of CD8+ mediated cell killing: | CTls recognize infected cell w/ class I MHC-> release perforin and granzymes which are endocytosed-> perforin releases granzymes-> granzymes cleave caspases->caspases induce apoptosis |
| Developing T cells are found where? | thymus |
| Developing B cells are found where? | bone marrow |
| What is responsible for developing peripheral self-tissue antigens for thymic APCs to show T cells? | AIRE autoimmune regulator protein |
| If a T-cell has a high affinity for self-antigens what 2 things can happen? (ideally) | negative selection or if it is CD4+ can become a Treg Cell |
| If a B-cell strongly recognizes a self-antigen, ideally, what 2 things can happen? | induce receptor editing or apoptosis |
| Example of T-cell Second Signal and 2 costimulators | CD28; B7-1 and B7-2 |
| 2 inhibitory receptors involved in T-cell anergy | CTLA-4 and PD-1 |
| Peripheral Tolerance:? Name 3 ways and which cells are involved. | Anergy: T-and B cells; Suppression byT-regulatory cells; activation induced cell death of CD4+ T-cells and B cells |
| T-regs have what 3 things | CD25, IL-2 receptor, Foxp3 |
| Name of severe autoimmune disease that results from Foxp3 mutations | IPEX |
| Polymorphiisms in CD25 are linked to what disease | Multiple Sclerosis |
| What is CD95 | Fas |
| What cells display Fas ? | many cells |
| What cells display Fas-L? | Activated T-cells |
| Human disease caused by Fas mutation? | autoimmune lymphoproliferative syndrome |
| 3 “immune privileged” sites | Testes; brain; eye |
| Genes most contributory to autoimmune predisposition | HLA |
| Polymorphisms in this gene are associated with RA, DM type 1, and others. Most frequently implicated mutations | PTPN-22 |
| Polymorphisms in NOD-2 contributes to what disease | Crohn disease |
| Mutations in these two genes are associated with MS and others | IL-2 receptor(CD25); IL-7 receptor α-chain |
| Name associated with new Ag from inside tissues not normally scanned by the immune system having lymphs that now recognize and attack these self-Ag | epitope spreading |
| Predominant damage caused by macrophages results from mediation by these cells | TH1 cells |
| Predominant damage caused by neutrophils and monocytes results from mediation by these cells | TH17 cells |
| Population SLE is most common in: sex? Age? Race? | black and Hispanic women age 20-30 |
| Most common Ab in SLE | Generic ANA |
| 2 Most diagnostic SLE Ab? | Anti-dsDNA and Smith Ag |
| Some SLE Pt’s will have a false positive in serology testing for what disease? What is the Ab causing it? | Syphilis; anti-phospholipid-β2-glycoprotein complex Pt has hypercoagable state, multiple spontaneous miscarriages; focal cerebral ischemia w/ anti-dsDNA Ab Dx? w/o anti-ds DNA Ab or ANA Dx? |
| Pt has Scl-70 and Anticentromere Ab. Dx? | Diffuse Systemic Sclerosis aka Scleroderma |
| Anticentromere Ab is specific for what Dx? | CREST |
| SS-A (Ro) and SS-B(La) Ab are specific for what Dx? | Sjogren Syndrome |
| Antihistone Ab is very specific for what Dx? | drug induced Lupus |
| Ab toward for histidyl-tRNA synthase; Jo-1 Ab is specific for what Dx? | Inflammatory myopathies |
| 5 classes of SLE nephritis in order | Minimal Mesangial; Mesangial Proliferative; Focal Proliferative; Diffuse Proliferative; Membranous |
| Distinguish Class III vs IV | III <50% glomeruli are involved; IV is the most severe |
| Specific morphology of Type IV SLE nephritis | >50% glomeruli; crescents fill Bowman’s Space; hematuria, proteinuria, HTN, Renal insufficiency |
| Pt with SLE and diffuse thickening of renal capillary walls has “Wire Loop”. What does this tell you? | Usually Type III or IV and ACTIVE DISEASE |
| If you expect SLE and Pt has other Sxs. What would the malar skin look like? | vacuolar degeneration of basal epidermal layer, complexes at dermalepidermal junction |
| Autopsy: vegetations on heart valve leaflets. SLE vs RA | SLE vegetations are larger, and on all surface of the leaflet vs on closing line in RA |
| Spleen in SLE Pt | Splenomagaly, capsular thickening, onion skin arteries |
| MCC of death in SLE | renal failure with intercurrent infection |
| 23yo BF Pt with skin plaques with raised erythematous boarders on face and head. No systemic involvement. ANA positive, anti-dsDNA negative, anti-histone negative. Dx? | Chronic Discoid Lupes Erythematosus |
| 23yo BF Pt with widespread erythematous skin rash, hematuria, pain in fingers and feet with no deformity, anti-SS-A positive, anti-histone negative. Dx? HLA genotype? | Subacute Cutaneous Lupus Erythematosus; HLA-DR3 |
| 23yo BF Pt has bilateral feet and hand pain with no deformities, fever. Normal neuro and renal. Pt is a missionary returning from Africa. Anti-dsDNA Negative. Dx? Serology? HLA type? | Drug Induced Lupus Erythematosus 2ndary to isoniazid; anti-histone positive; HLA-DR4 |
| 2 most common Sxs of Sjogrens | xerostomia, keratoconjuctivitis sicca (dry eyes) |
| Suspect Sjogren’s Pt’s also have? | RA |
| Sjogren’s: Decrease in tears and saliva are from | lymphocytic infiltrate and fibrosis of the lacrimal and salivary glands |
| 4 Ab in Sjogren’s | ANA; SS-A; SS-B; Rheumatoid factor (anti-self IgG) |
| Most important Ab in Sjogren’s, high levels predispose to earlier onset, longer duration, extraglandular involvement | anti SS-A |
| 2 viruses possibly associated w/ Sjogren’s. 1 that can mimic Sjogren’s. | EBV, HCV; HTLV-1 can clinically and pathologically mimic |
| Earliest morphologic change in Sjogren’s | periductal/perivascular lymphocytic infiltration |
| Mechanism: Progression of Damage in Sjogren’s | lymph infiltrate becomes extensive->follicles w/ germinal cells in large salivary glands-> ductal epithelial hyperplasia->acini atrophy->fibrosis-> atrophy->steatotic change |
| Sjogren’s presents most commonly in? | 50-60yo women |
| Renal Changes in Sjogren’s vs SLE | no glomerular lesions in Sjogren; tubulointerstitial nephritis w/ renal tubular acidosis |
| Who is more likely to experience extraglandular Sxs? What are they? | High SS-A titer; diffuse pulmonary fibrosis, peripheral neuropathy, tubulostitial nephritis |
| Even with SS-A and SS-B, and ANA, what is done to confirm dx? | lip biopsy |
| Difference in Diffuse vs Limited Scleroderma | Diffuse: Widespread skin involvement, early visceral involvement, rapid progression |
| What can Pt’s with Limited Scleroderma develop and what is a marker for it? | CREST syndrome; anti-centromere Ab |
| Ab associated with Diffuse Scleroderma | everyone has ANA; anti Scl-70 (DNA topoisomerase) |
| What is associated with limited scleroderma and anti-centromere Ab? Sxs? | CREST syndrome; Calcinosis, Reynaud’s phenomenon, Esophageal dismotility, sclerodactyly, Telangiectasia |
| Early morphological hallmark of Scleroderma | microvascular disease; intimal proliferation of digital arteries; capillary dilation and leaking |
| 2 measurable levels pointing to endothelial and platelet activation in scleroderma | increased vWf; increased circulating platelet aggregates |
| In addition to vascular injury, what else adds to the pathogenesis of scleroderma | fibroblast activation |
| Change seen in vascular smooth muscle in Scleroderma | increased adrenergic receptors |
| 4 prominent areas of change in systemic scleroderma | Skin, alimentary tract, MS system, kidney |
| Skin changes in systemic scleroderma | strophy starts distally moves proximally from fingers; perivascular CD4+ infiltrates; fibrosis of the dermis with “drawn mask face”, cutaneous ulceration, autoamputation of fingers |
| Most prominent changes in Ailimentary tract in systemic scleroderma | lower 2/3 of esophagus develops “ruber hose inflexibility; LES dysfunction, GERD; loss of micro/villi in small bowel=malabsorption |
| Fibrosis of joints occur in Scleroderma but what differentiates it from RA? | Joint destruction is rare |
| Kidney changes in scleroderma resemble what other process? What differentiates them | malignant HTN; Scleroderma changes (mucin/collagen-ous intimal thickening only of 150-500um vessels |
| Pulmonary changes in Scleroderma is indistinguishable from this process? | Idiopathic Pulmonary Fibrosis |
| MC Systemic Scleroderma presents in? distinguishing feature | 50-60yo BF; cutaneous change |
| This is the first sign of Systemic Scleroderma in 70% of people. | Reynaud’s Phenomenon |
| Rapid deterioration of Pt with Systemic Scleroderma, resulting in death. MCC? | Malignant HTN with fatal renal failure |
| Pt was told she had symptoms of SLE. Had mild renal involvement that resolved when you gave her corticosteroids. High titer of Ab to ribonucleoprotein particle (RNP)- containing U1 ribonucleoprotein. Dx? And 2 serious complications | Mixed Connective Tissue disease; pulmonary HTN, Renal disease like systemic sclerosis |
| APC involved is the Pt’s: Direct or Indirect Pathway of Tissue Rejection? | Indirect |
| APC involved is in the graft: Direct or Indirect Pathway of Tissue Rejection? | Direct |
| Activated CD8+ cells that can directly injure graft tissue can only be activated in the Direct or Indirect Pathway of Tissue Rejection? | Direct |
| Which is the major pathway of acute cellular rejection, Direct or Indirect Pathway of Tissue Rejection? | Direct |
| Which pathway is the major pathway involved in chronic rejection, Direct or Indirect Pathway of Tissue Rejection? | indirect |
| Rejection of graft that happens in minutes or hours after transplant? What is the causative agent? What branch of immunity is involved? | Hyper acute rejection; pre-formed antidonor Ab; humoral immunity |
| Acute humoral rejection targets what, predominantly for injury in the graft | graft vasculature |
| Upon removal of a rejected kidney there is Ig and Compliment in vessel walls, endothelial damage, neutrophils, and platelet + thrombin thrombi. Dx? | Hyperaccute rejection |
| Rejection of kidney in first month. Interstitial and glomerular and peritubular mononuclear cells, CD4 and CD8+; focal tubular necrosis and vascular endothelial cell injury. Dx? | Acute Cellular Rejection |
| Reason recognizing Acute Cellular Rejection with no Humoral Rejection is important. | Treatment with immunosuppression is very well tolerated and has good response |
| Rejection of kidney in first month. Thickened vascular intima with fibroblasts, myocytes, and foamy macrophages; small areas of renal cortical infarction and atrophy. Neutrophillic infiltrates. Dx? | Acute humoral rejection |
| What can you find that is a strong correlation to Humoral rejection, that will be deposited in allografts? How is it formed? What can you treat with if this is found? | CD4d; classical pathway activation of the compliment system; treat with B-cell depleting agents |
| Rejected kidney. Obliterative intimal fibrosis in cortical arteries, renal ischemia, shrunken parenchyma, duplication of glomerular basement. Interstitial plasma cells and eosinophils Dx? | Chronic Rejection |
| Mainstay in immunosuppressive drugs | cyclosporine |
| MOA of cyclosporine | blocks NFAT; prevents cytokine production namely IL-2 |
| 3 locations of common Acute GVH attacks and Sxs | skin epithelia, desquamating rash; liver, small bile duct destruction w/ jaundice; ulceration of the intestine, bloody diarrhea |
| 4 locations of common Chronic GVH attacks and Sxs | skin, destruction of skin appendages and fibrosis; esophageal strictures, liver, cholestatic jaundice; lymphnodes, depletion of lymphocytes |
| Step taken to mediate GVH? Adverse effects of this step? | deplete Donor T-cell population prior to transplant; EBV related B-cell lymphoma and graft rejection increases |
Created by:
csheck
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