Immunology/Inflammation/Vaccines Flashcards by Karolina Kowalczyk

What do COX-1 and COX-2 Inhibitors inhibit?

Cyclooxygenase (and therefore, thromboxane)

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What cytokines are responsible for activating the anti-viral state in cells?

Type 1 IFNs

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profound block in T cell development

Se vere combined Immunodeficiency (SCID)

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What hypersensitivity is this?

Immune Thrombocytopenia - autoantibodies against protein antigens on platelet surface (NO INFLAMMATION)

Type II

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The kinin cascade leads to the formation of what? Function?

Bradykinin - vasoactive

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Lack of gamma chain (X-linked) or JAK3 (autosomal recessive) leading to lack of cytokine signaling (type of SCID)

Cytokine signaling deficiency

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What hypersensitivity is this?

Graves Disease - autoantibody binds to TSH receptor —> activates receptor and causes inappropriate production of thyroid hormone

Type II

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The clotting system leads to the formation of what? Function?

Thrombin and fibrin - clotting

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What hypersensitivity is this?

Systemic Lupus Erythematosus (SLE) - cause by wide array of auto-antibodies leading to immune complex deposition

Type III

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What hypersensitivity is this?

Myasthenia Gravis - autoantibody binds to Ach receptor; blocks Ach binding resulting in perceived muscle weakness; no inflammation

Type II

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MHC II presents to which cell? What about MHC I?

MHC II: CD4+

MHC I: CD8+

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What hypersensitivity is this?

anti-GBM; Goodpasture Syndrome - Autoantibodies against portion of collagen in glomerular and alveolar capillary membrane —> kidney inflammation and hemorrhage

Type II

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Th1 CD4+ stimulates what?

Phagocytosis of microbes
IFN-gamma for macrophage activation
IgG production
Opsonization

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Abnormal fibrils are produced when soluble precursors undergo conformational change and aggregate; Fibrils are deposited into extracellular tissues and disrupt normal function

Amyloidosis

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accumulation of adenosine, resulting in premature death of lymphocyte precursors

ADA deficiency

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What are the following antibodies responsible for: IgA, IgE, IgG, IgM?

IgA - mucosal immunity
IgG - everything; Th1 activated
IgE - allergies/mast cell degranulation; Th2 activated
IgM - classical pathway of compliment

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What hypersensitivity is this?

Autoimmune Hemolytic Anemia - autoantibodies against protein antigen on RBC surfaces

Type II

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block in granulopoesis (neutrophil production)

Severe congenital neutropenia

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What are the secondary lymphoid organs?

Lymph nodes, spleen, mucosal and cutaneous lymphoid tissue

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What are the co-stimulating receptors on T cells?

B7 - CD28

CD40L - CD40

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A severe immunodeficiency due to lack of phagocyte oxidase

Chronic granulomatous disease (CGD)

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An inherited deficiency in adhesion molecules required for cell migration; results in decreased innate immunity

Leukocyte adhesion deficiency

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How can monoclonal bodies be used to target tumor cells?

Act as checkpoint inhibitors (CTLA-4 and PDL/PDL1) to maintain T cell function against tumor

What hypersensitivity is this?

Rheumatoid Arthritis - chronic inflammatory disease of the joints/synovial cells (synovitis) via TNF and IFN

Type IV

What are the main mediators of leukocyte recruitment?

Selectin Integrin PECAM-1 Chemokines

BTK gene deficiency, decreased pre-B cell signaling

X-linked agammaglobunlinemia

What cytokines are responsible for inflammation?

TNF, IL-1

What does the hyperactute rejection of an organ rely on?

Already circulating alloantibodies

Th2 CD4+ stimulates what?

``` Eosinophil-mediated immunity against helminths Release of IL-4, IL-5, and IL-13 for mast cell/eosinophil activation IgE production (allergies) ```

If free antigen gets into the blood, where does it trigger an immune response?

Spleen

What are monoclonal antibodies?

genetically engineered antibodies that are very specific for one target; can remove one cell type or protein

What cytokines are responsible for chemotaxis?

CXCL8

lack of CD40L, leads to deficiency of IgG, IgA, IgE

Hyper-IgM

What are the primary effector mechanisms of the immune system?

Phagocytosis Membrane Attack Complex Cytotoxicity Neutralization

What happens during direct acute organ rejection?

1. Graft has an APC 2. Donor MHC I/II antigens on APCs in the graft are recognized by CD8+ and CD4+ cells 3. CD4+ cells proliferate/produce cytokines —> cause damage via delayed-type hypersensitivity 4. CD8+ cells directly kill graft cells

What happens during indirect acute organ rejection?

1. recipient’s APCs presents graft antigens, which activates CD4+ T cells 2. CD4+ damage graft via local delayed type hypersensitivity (cytokines + macrophages) 3. B cells are stimulated by CD4+ to make antibodies

What two checkpoints on T cells do tumors target? What are their normal functions?

CTLA-4 - inactivates T cell (negative signal) | PD-1 - inhibits TCR-mediated response and T cell survival

Surface proteins used to define a specific cell type

Cluster of Differentiation

What endogenous factors limit inflammation?

Short life-span of mediators IL-10 and TGF-beta (anti-inflammatory) Lipoxins CTLA4 (inhibitory receptor on T cells)

What is Type II Hypersensitivity?

Cell/antibody-mediated: Antibodies bind to surfaces of cells and cause: - opsonization/phagocytosis - interference with protein function - Fc/complement activation

What do steroid inhibit and how does it differ from COX-inhibitors?

Phospholipases from making arachidonic acid, thus lipoxin/leukotriene Steroids inhibit both inflammation AND immune function where as COX-inhibitors only inhibit inflammation

Th17 CD4+ stimulates what?

Inflammation Recruitment of phagocytes for elimination of bacteria/fungi Release of IL-17 for neutrophilic/monocytic inflammation

What hypersensitivity is this? Diabetes Mellitus - direct killing of pancreatic beta cells (insulin secreting cells)

Type IV

What cytokines are responsible for activating liver synthesis of acute-phase proteins?

IN-6

What is Type IV Hypersensitivity?

Delayed T-cell mediated: 1. CD4+ T cells recognize antigen presented by APCs leading to generation of effector and memory TH1 cells 2. Subsequent exposure to antigen results in TH1 activation and release of cytokines —> macrophages, neutrophils —> tissue injury OR No mediator; intracellular peptide is presented by MHC I to CD8+ —> subsequent direct killing by CTL

characterized by aggregates of activated macrophages with scattered lymphocytes during certain pathological states; formation of granuloma walls off pathogen but does not always eradicate them

Granulmatous inflammation

What pathways does the Hageman Factor trigger?

Clotting cascade Kinin system Complement Fibrinolytic systems

Improper thymus development; deceased production of T cells

DiGeorge Syndrome

What is Type III Hypersensitivity?

Immune-complex-mediated: immune complexes form in the circulation between antigens and free body; deposit on vessel walls/joints/kidneys and lead to localized inflammation

What are the primary lymphoid organs?

Bone marrow and thymus

Competent T cells transplanted into recipient who is immunocompromised —> Activation of CD4+ and CD8+ T cells, with cytokine and cell-mediated tissue injury

Graft vs Host Disease (GVHD)

The fibrinolytic system leads to the formation of what? Function?

Plasmin - limits clotting and activates compliment

What are the 4 types of hypersensitivities?

A - allergic/anaphylactic/immediate (IgE) - I C - cell-mediated/antibody-mediate (IgM, IgG) - II I - immune-complex mediated (IgM, IgG) - III D - delayed T-cell mediated (CD4+/CD8+) - IV

What two receptors are involved in the Death Receptor pathway of apoptosis?

TNF | Fas

deficiency of one Ig subtype (usually IgA)

Hypogammaglobulinemia/CVID

What is the primary factor driving the diversity of the adaptive immune system?

Lymphocyte antigen receptor diversity