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Path 6 Immuno

LECOM Path Ch 6 Immunology

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