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Pathology > Immuno > Flashcards

Immuno Flashcards

1
Q

Role of:

  1. IL-1?
  2. IL-6?
  3. IL-8?
  4. IL-10?
  5. IL-12?
A
  1. cell activation, fever, production of acute phase protiens
  2. fever, production of acute phase proteins, activates B and T cells
  3. Neutrophil chemoattractant
  4. (anti-inflammatory) suppresses CMI-promoting cytokine production
  5. Activates NK cells (to make IFNgamma), TH0-TH1 polarization, activates Tc cells
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2
Q

Role of:

  1. IL-17?
  2. TNFalpha?
  3. IFNalpha/beta?
  4. IFNgamma?
  5. IL-2?
A
  1. activates neutrophils, fibroblasts, and keratinocytes
  2. Iike IL-1 plus induces chemokine production from macrophages and endothelial cells and induces class one expression. At high concentrations causes cachexia, inhibits myocardial contractility, and smooth muscle tone resulting in hypotension (no shock with TGFbeta)
  3. antiviral, increase Class I expression, promotes TH0–>TH1 polarization
  4. cell activation, Class I and II expression, promotes IgG isotype switching, and promotes CMI (activates Tc, TH1, NK, and macrophages)
  5. promotes T cell maturation and growth; activates Tc and NK cells
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3
Q

Role of:

  1. IL-4?
  2. IL-5?
  3. IL-13?
  4. IL-3?
  5. IL-7?
A
  1. Promotes IgE isotype switching, mast cell and eosinophil activation, and suppresses macrophages
  2. promotes eosinophil maturation and activation and IgA isotype switching
  3. inhibits the synthesis of proinflammatory cytokines from macrophages and promotes IgE production
  4. Induces B cell and granulocyte maturation
  5. Induces B and T cell maturation
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4
Q

Role of:

  1. GM-CSF?
  2. G-CSF?
  3. M-CSF?
  4. TGFbeta and IL-10?
A
  1. eosinophil, neutrophil, and monocyte maturation
  2. neutrophil maturation
  3. monocyte maturation
  4. Inhibits TH1, TH2, and TH17 activities
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5
Q
  1. Where do you find MHC I? II?
  2. Functions of MHC?
  3. Structure of MHC I? II?
  4. Ag processing of MHC I? II?
  5. What cells have TLR?
A
  1. all nucleated cells and platelets; surface of APCs
  2. Distinguish self from non-self, bind peptide Ags and present them to T cells
  3. Polymorphic alpha and nonpolymorphic B; polymorphic alpha and beta
  4. Intracellular: proteolytic degradation –> ER –> assembly –> expressed on surface. Extracellular: endocytic uptake –> endosomes –> vesicle to surface
  5. dendritic cells, macrophages, NK, B, T, mucosal epithelial cells and endothelial cells
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6
Q
  1. What does TLR 1 bind? TLR 2? TLR 3? TLR 4?
  2. What cytokines are produced during the acute phase response?
  3. Natural killer type of response (innate/adaptive)? What do they respond to?
  4. How are NK cells distinguished from T cells?
  5. NK cells express CD16 - play a key role in?
A
  1. bacterial lipopeptides; peptidoglycan, lipotechioic acid, and fungal wall components; dsRNA from viruses; LPS
  2. TNF, IL-1, IL-6
  3. innate to intracellular pathogens and tumors
  4. They dont express TCR/CD3 complexes
  5. Ab-dependent cell-mediated cytotoxicity (ADCC)
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7
Q

NK cells

  1. What are their inhibitory vs activating receptors?
  2. Activated cells secrete?
  3. What 2 cytokines induce NK proliferation and increase activity? Also enhanced by?
  4. How do NK cells lyse Target cells?
A
  1. Inhibitory (CD94) engage MHC I on normal cells; Activating receptors bind poorly defined ligands on infected to tumor cells
  2. IFNgamma, GM-CSF, TNFbeta
  3. IL-12 and IL-15; IFNgamma, IL-1, IL-2
  4. By degranulation, releasing perforin and granzymes that induce target cell apoptosis
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8
Q
  1. NKT cell subclasses? Produce?
  2. NKT cell function?
  3. Antibodies - what chain is variable? constant
  4. What induces THO–> TH1 polarity? TH2?
  5. TH2 can induce the formation of what immununoglobulins?
A
  1. CD4+: produce TH2 and TH1 cytokines CD4-: produce IFNgamma and IL-2 only
  2. Kill cells by expressing lipid Ags and promote CMI and/or Ab production
  3. light; heavy
  4. IL-12; IL-10
  5. IgE via IL-4/IL-13; IgA via IL-5
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9
Q
  1. TH1 with IFNgamma induces?
  2. TH1 with IFNgamma, TNFbeta, and IL-2 induces?

MALT

  1. What does MALT consist of?
  2. How is Ag entry mediated?
  3. Plasma cells here secrete?
  4. What are the free cells?
A
  1. IgG isotype switching
  2. T helper cells
  3. Aggregates of non-encapsulated lymphoid tissue in the LP and submucosa
  4. M cells that create pockets with B, T, dendritic cells and macrophages
  5. IgA
  6. LP lymphocytes (CD4), B cells, plasma cells, and transepithelial lymphocytes (CD8)
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10
Q

B cells

  1. Mature where? Require what? What other cell matures here?
  2. Adhesion molecules and what they bind to?
  3. Signal transduction and binding?
  4. Ag presentation? Processing?
A
  1. Bone marrow; IL-3 and IL-7; NK cells
  2. ICAM1 to LFA-1 (on T cells) and LFA3 binds to CD2 (on T cells)
  3. CD40 to CD40L on T cells, B7.5 binds CD28 on T cells
  4. MHC II; Ag receptor, complement receptor, and Fc receptor
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11
Q
  1. Regulatory B cells produce?
  2. Effector B cells 2 are activated by? Produce?
  3. Effector B cells 1 are activated by? Produce?
  4. T cells: mature where? Require what? What other cell matures here?
  5. Where do you find CD4 cells? Bind to MHC ___.
  6. Where do you find CD8 cells? Bind to MHC ___.
A
  1. IL-10 and TGFbeta
  2. TH2; IL-2/4/6 and TNF alpha
  3. TH1; IL-12, TNF alpha, and IFNgamma
  4. Thymus; IL-2/7 and thymic hormones; NKT cells
  5. T-helper cells; MHC II
  6. Cytotoxic T cells; MHC I
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12
Q
  1. T cell antigen receptor is composed of? Accessory molecules associated with transduction and cell activation?
  2. CD28 binds to what? Function?
  3. CD154 binds to what? Function?
  4. Adhesion molecules and binding?
  5. CD4: What causes polarization to TH1?
A
  1. TCR (2 subunits) associated with Ag recognition; CD3 and zeta
  2. CD80/86 on APCs; costimulatory second signal
  3. CD40 on APCs; causes a third signal
  4. CD2 binds LFA3 on APC, LFA1 binds to ICAM-1 on APC and endotheium
  5. Ag, IL-12, and IFNgamma
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13
Q
  1. TH1 secretes? Function?
  2. What induces TH2 polarization?
  3. TH2 secretes? Function?
  4. What causes polarization to TH17?
  5. TH17 secretes? Function?
  6. CD8 pre-Tc cell requires what to become lytic?
A
  1. CMI: IL-2/3, GM-CSF, TNFbeta; IFNgamma: isotype switching to IgG
  2. Ag, IL-4/10
  3. IL-2/3, GM-CSF, IL4/5/13: isotype switching and B cell proliferation
  4. Ag, IL-6/1, and TGFbeta
  5. IL-17 (neutrophil recruitment/survival) and IL-22 (activates keratinocytes and fibroblasts to secrete IL6/8 and induce MHC I on keratinocytes)
  6. Ag, IL-2, and IFNgamma
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14
Q

Regulatory T cells

  1. Function of IL-10?
  2. Function of TGFbeta?
  3. Monocyte/macrophage function?
A
  1. Inhibits IL-12 production from macrophages/dendritic cells –> blocks development of TH1 phenotype and CMI, also inhibits MHC II expression on the same cells
  2. Inhibits T cell/macrophage activation, increases IgA production, stimulates CT production and angiogenesis
  3. Ag processing, control TH1 (secretes IL-12) and TH2 (secretes IL-10) polarization, major cell type of CMI/DTH, tissue damage/reorganization/healing
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15
Q
A
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16
Q
  1. Interdigitating dendritic cells are the most important _____.
  2. Interdegitating dendritic cells begin as ___ cells that develop from ____.
  3. After antigen encounter where do DC migrate? What happens?
  4. Where are follicular dendritic cells found?
  5. What do follicular dendritic cells express? What dont they express? Function
A
  1. APC
  2. langerhans; macrophages
  3. draining nodes; mature and express increased MHC proteins to present Ag to Th cells
  4. First and second degree follicles of lymph nodes, spleen, and mucosal lymphoid tissue
  5. Receptors for Ab and compliment; MHC II (thus they are NOT APCs); hold immune complexes in lymphoid tissue
17
Q
  1. TH2 incudes by? Inhibited by?
  2. TH1 induced by? Inhibited by?

ALLERGY/HYPERSENSITIVITY

  1. Type I: ___ response to soluble Ag –> production of ___.

TYPE I

  1. TH2 cells produce what cytokines that induce IgE and Ab production?
  2. TH2 also produces IL-9: Function? IgE binds to __ cells and ____ via Fc.
A
  1. IL-4; IFNgamma and IL-12
  2. IFNgamma and IL-12; IL-4/10/13
  3. TH2; IgE
  4. IL4/10/13
  5. Activates mast cells; mast; basophils
18
Q

Type I hypersensitivity

  1. Local type one reactions are associated with what cells? 5 local reaction examples?
  2. Systemic reactions are associated with what cells? Examples?
  3. 2 mast cell types? Produce? Granules contain? Location?
  4. Degranulation mechanisms of mast cells?
  5. Primary mediators from mast cells and basophils?
A
  1. mast cells; urticaria, allergic rhinitis, asthma, atopic dermatitis, and food
  2. Mast cells and basophils; anaphylaxis
  3. Mucosal: leukotrienes and PGD2; chondroitin sulfate, intestines and lungs CT: PGD2; heparin; skin and intestines
  4. IgE bound to Fc –> cross linked by allergen –> induces phosphorylation and kinase recruitment –> PIP2 to DAG –> increased calcium and activated map kinase –> activates cytoplasmic PLA2 –> hydrolyzes PC to arachadonic acid –> metabolized to PGD2 and LTB4/C4/D4/E4. Also PKC is activated –> phosphorylates myosin –> granule release
  5. Histamine, tryptase, chymase, esoinophil and neutrophil chemotactic factors
19
Q

Type I hypersensitivity

  1. Histamine to H1 receptors causes?
  2. Histamine to H2 receptors causes?
  3. Tryptase (from both mast cells) induces? Chymase (from ___ mast cells) causes?
  4. Primary mediator cytokines from mast cells and basophils?
A
  1. Increase vascular permeability, smooth muscle contraction, increased mucus production
  2. muscle relaxation –> vasodilation, increased vascular permeability
  3. Bronchial hyperresponsiveness; CT, increased mucus production
  4. TNFalpha and IL-6 promote inflammation
20
Q

Secondary mediators

  1. Functions of LTB4?
  2. Effects of LTC4/D4/E4 depend on receptor: LT1 vs LT2?
  3. Functions of PGD2?
  4. Functions of PGE2?
  5. What is systemic anaphylaxis and local inflammation caused by?
  6. What promotes TH2 polariztion?
  7. Function of IL3/5 and GM-CSF?
A
  1. Neutrophil chemoattractant (also induces adhesion and degranulation)
  2. LT1: increased vascular permeability, bronchoconstriction LT2: endothelial activation
  3. vasodilation, increased vascular permeability, smooth muscle contraction, inhibits platelet aggregation, and is chemotactic for eosinophils and TH2 cells
  4. smooth muscle contraction, vasodilation, and increased vascular permeability
  5. IL1/6 and TNFalpha
  6. IL4/13
  7. Stimulates eosinophil production and activation
21
Q

Type I hypersensitivity

  1. What are non-mast cell mediators?
  2. Type I hypersensitivity yeilds a ___ response. What are the phases?

Anaphylaxis

  1. Atopic or non-atopic and why?
  2. Clinical features: skin? vascular? lungs? hemostatic?
  3. What is angioedema?
A
  1. prostacyclin, plasma kinin and fibrolytic cascades
  2. biphasic; early (primary mediators) and late (secondary mediators)
  3. non-atopic because there is no genetic predisposition
  4. pruritis, erythema, urticaria, and or angioedema; hypotension and shock; bronchial obstruction from mucosal edema, bronchospasm, increased mucus; activation of coagulation pathway (DIC)
  5. nonpitting edema without pruritis; deep dermis, subcutaneous, and or submucosal tissue
22
Q

Type I hypersensitivity

  1. Most common atopic hypersensitivity?
  2. Clinical manifestations of rhinitis?

Asthma

  1. What is it?
  2. Extrinsic asthma?
  3. Intrinsic asthma?
  4. Bronchial reactions: early vs late?
A
  1. allergic rhinitis
  2. watery rhinorrhea, sneezing, nasal obstruction, puruitic conjunctiva, “allergic shiners”
  3. reversible obstructive airway disease characterized by hyper-responsiveness
  4. Atopic: IgE and allergen related, +skin test, family history, increased serum IgE and begins early in life
  5. -skin test, no family history, later in life, vagal response to environmental irritants
  6. Early: mast cell and eosinophil primary mediators - smooth muscle contraction, vasodilation, edema, and increased mucous production Late: eosinophils/neutrophils - thick mucus plugs, mucosal edema, bronchoconstriction
23
Q
  1. What occurs in chronic asthma inflammation?
  2. What are the acute asthmatic symptoms? Chronic?

Atopic Dermatitis

  1. Often accompanies ____ respiratory allergy.
  2. Acute lesions? Chronic lesions?
  3. Treatment?
A
  1. basement membrane thickening, smooth muscle hyperplasia, and hypertrophy
  2. acute: dyspnea, wheezing, cough, increase pulse, shortness of breath chronic: bronchial thickening and lumen obstruction
  3. atopic (extrinsic)
  4. acute: vesicular/pruritic on face/flexors with symmetric distribution, and itching chronic: dry and scaly, epidermal hyperplasia, hyperkeratosis
  5. moisturizer, antihistamines, steroids, topical tacrolimus
24
Q

Type II Hypersensitivity

  1. What is it?
  2. Components involved?
  3. For cytotoxic Ab rxns: IgG/IgM is made to what Ags?
  4. Ab binds and activates ____ causing destruction. C3b opsonization may increase ___. Bound Ab may increase cell lysis by _____.
A
  1. IgM/IgG response to cell or matrix associated ag/receptor resulting in inflammation and destruction/altered receptor signaling
  2. IgG, IgM, complement, T/B/NK cells, neutrophils, and macrophages
  3. intrinsic or tissue bound Ags
  4. complement; phagocytosis; ADCC
25
Q
A
26
Q

Type II hypersensitivity

  1. Compliment activation and nutrophil recruitment result in ___-mediated tissue damage. Ab to tissue Ags may also cause __ receptor-mediated leukocyte recruitment.
  2. What is hemolytic anemia? How is it assessed?
  3. 3 classifications of anemia?

HA

  1. What is often seen with RBC lysis?
  2. How does the kidney respond? Bone marrow?
  3. How do the RBCs look?
  4. Symptoms/signs? Explain
A
  1. inflammation; Fc
  2. Reduction in RBC count, hematocrit, and/or hb concentration; measure RBC count, mean cell vol, Hb, and hematocrit
  3. Blood Loss, increase rate of destruction (intrinsic = hereditary), impaired production
  4. Increased LDH/Hb/bilirubin
  5. Increased production of EPO by kidney and BMarrow stimulates erythroid hyperplasia –> reticulocytosis
  6. normochromic and normocytic –> spherocytosis
  7. Jaundice (from bilirubin in tissue), splenomegally (collection of RBC in the spleen), and fever (from systemic inflammation)
27
Q

Type II hypersensitivity

Erythroblastosis fetalis

  1. Type of HA? What occurs?
  2. Symptoms? Treatment? Prevention?
  3. Autoimmune cold HA: how is it acquired? What is the Ab? Symptoms are mild
  4. Secondary cold HA: how acquired? Ab?
  5. Paroxysmal cold HA: characterized how? acquired? Ab?
A
  1. warm immune HA; Rh- mom gives birth to Rh+ baby; from second pregnancy IgG crosses placenta and causes fetal HA
  2. Jaundice/anemia/hepatosplenomegaly; transfusions, anti-Rh administered within 72 hours of first child born
  3. Idiopathic; IgM binds surface RBC Ags
  4. Post infectioous (mycoplasma pneumonia, mono, malignancy); IgM
  5. Sudden onset and often recurrent; post infectious or autoimmune; IgG
28
Q

Type II hypersensitivity - immune thrombocytopenia

  1. What are these conditions associated with?
  2. General clinical manifestations?
  3. Autoimmune type: chronic or acute? Population? Onset? How acquired?
  4. Drug induced: what drugs?

Secondary immune thrombocytopenia

  1. In kids, associated with? Onset?
  2. Adult association? Examples
A
  1. Increased platelet destruction from anti-platelet IgG
  2. Purpura, petichiae, ecchymoses (from minor trauma or spontaneous), epistaxis and hemorrhagic bullae, anemia, chills, fever
  3. Chronic; older adults; gradual onset; (self limiting) idiopathic
  4. aspirin, abx, diuretics
  5. Viral post infection; acute onset and self limiting
  6. Autoimmune diseases: lupus, leukemia, lymphoma, HIV
29
Q

Type II tissue - associated diseases

Anti-GBM nephritis

  1. What is this disease?
  2. MOA?
  3. Clinical manifestations are that of Acute nephritic syndrome: what are they?
  4. Pathologic change is RPGN: what is this? What are formed and how? What is prominent between cellular layers? What happens to bowmans space?
A
  1. Autoimmune disease involving production of Ab to an epitope in Type IV collagen of GBM
  2. Ab binds to GBM –> activated compliment/neutrophils/other inflammatory cells –> damage to BM
  3. impaired filtration –> hematuria, proteinuria, edema, and hypertension
  4. Rapidly progressive GN; crescents by inflammation induced proliferation of parietal cells; fibrin and fibronectin; obliterated and tuft is compressed
30
Q

Goodpastures Syndrome

  1. What is this?
  2. Pathogenesis?
  3. Symptoms?
  4. What is myasthenia gravis? Often occurs with? (related to thymus)
  5. MG: immunopathogenesis?
  6. MG: symptoms? Crisis?
A
  1. Pulmonary hemorrhage syndrome often following a viral infection
  2. binding of Abs to the ABM and GBM followed by compliment and inflammation
  3. pulmonary first with hemorrhage: cough, hemoptysis and dyspnea, then RPGN (w/ crescents, inflammation, and fibrin/fibronectin)
  4. Abs to ACh receptors; thymic hyperplasia (thymoma)
  5. Acute Ab interrupts transmission by increasing endocytosis of receptors, also, compliment is activated resulting in postsynaptic membrane damage
  6. proximal muscle weakness, hard to climb stairs/hold head up/swallow; involve breathing muscles
31
Q

Type II Hyperthyroidism

  1. What occurs?
  2. Pathology?
  3. Symptoms of thyrotoxicosis?
  4. Symptoms specific to graves?
A
  1. Auto-Ab to TSH receptor: stimulates brain to cause increased production of TH
  2. Epithelial hyperplasia and enlarged gland
  3. Nervousness, emotional issues, tachycardia, GI hypermotility, weakness and muscle atrophy, warm moist skin, heat intolerance, weight loss
  4. ophthalmopathy involving periorbital edema early followed by fibrosis (exopthalmos)
32
Q

Type II

Bullous Pemphigoid

  1. Immunopathogenesis?
  2. Inflammatory infiltrate? What does this induce?
  3. Symptoms?
A
  1. Auto-Ab to Ags at dermal-epidermal junction and activation of compliment
  2. Eosinophils and lymphocytes; dermal-epidermal separation and blisters
  3. Fluid filled blisters on flexors of extremities, axilla, groin, and lower abdomen
33
Q
  1. Pemphigus Vulgaris - immunopathogenesis?
  2. Pemphigus Vulgaris - symptoms?

Pernicious Anemia

  1. Pathogenesis?
  2. How does the gastritis occur?
  3. What are the Abs?
  4. Bone marrow/blood manifestations?
  5. Stomach manifestation?
  6. CNS manifestation?
A
  1. Auto-Ab binds to the epidermal cell adhesion molecules and causes them to separate via acantholysis (lysis of intercellular adhesion sites)
  2. Affects mucosa, scalp, chest, and body folds with flaccid blisters that crust and rupture
  3. Autoimmune destruction of gastric mucosa resulting in gastritis and decreased B12 absorption
  4. Mostly CD4 T cells cause a loss of parietal cells with decrease in intrinsic factor production and decrease in acid production
  5. 2 autoabs - one blocks binding of B12 to intrinsic factor and another blocks IF binding to ileal cells
  6. Megaloblastic anemia with leukopenia, thrombocytopenia, and mild jaundice
  7. gastritis, mucosal atrophy, increased incidence of cancer
  8. Demyelination - spastic paraparesis (weakness), ataxia, and parasthesia

Pathology (11 decks)

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