Hd Test 1 - Innate Immunity

Front 1

Neutrophils

Back 1

phagocytic granulocytes that respond to chemotactic signals, clear bacterial/fungal infections. 70% of all WBC

Front 2

Neutrophil receptors

Back 2

CD14 and TLR4 (lipopolysaccharides of gram-neg bacteria); C3 and C4 complement receptors; scavenger, mannose, glycan. FcR for Ig bound to bacteria.

Front 3

Neutrophil storage and release

Back 3

stored in bone marrow; enter bloodstream when signaled by macrophages when needed to fight infection.

Front 4

Extravasation

Back 4

rolling adhesion, tight binding, diapedesis, migration

Front 5

oxygen-independent phagocytosis

Back 5

microbe engulfed in phagosome; vesicles and 3 types of granules fuse w/ it and release degradative enzymes to kill pathogen/lower pH.

Front 6

oxygen-dependent phagocytosis

Back 6

Free radicals form w/in phagolysosome; ROI from NADPH-dep oxidases and RNI from iNOS

Front 7

Respiratory burst

Back 7

consumption of oxygen in neutrophils to produce free radicals.

Front 8

glucose-6-phosphate dehydrogenase deficiency

Back 8

defective NADPH production >> impaired respiratory burst >> chronic bacterial and fungal infections

Front 9

leukocyte adhesion deficiency

Back 9

impaired migration of phagocytes to infected tissues >> widespread capsulated bacterial infections

Front 10

Eosinophils

Back 10

Kill helminthic parasites; 1-6% of all WBC's

Front 11

Eosinophil storage

Back 11

Most stored in bone marrow until needed; some reside in CT of respiratory, GI and urogenital tracts.

Front 12

Eosinophil function

Back 12

When activated, its IgE receptor can bind IgE bound to parasites. Release enzymes, proteins, cytokines, chemokines. Very toxic, so few are found in systemic blood.

Front 13

Basophils

Back 13

Promote inflammatory response; <1% of all WBC

Front 14

basophil function

Back 14

Fc receptors can bind IgE >> release histamine; promotes inflammatory response and participates in allergic rxn

Front 15

Mast cells

Back 15

Responsible for many allergy/asthma symptoms. 2 types: mucosal and CT.

Front 16

Mast cell function

Back 16

found in skin, CT, mucosa, respiratory tissue; Fc receptors bind IgE and release histamine, heparin, etc.

Front 17

NK cells

Back 17

large granular lymphocytes that are found in the bloodstream and mediate early response to infection. destroy virally-infected cells and some tumor cells. Release IFN-gamma

Front 18

NK activation

Back 18

by Il-12 and TNF-alpha from macrophages and IFN alpha/beta from virally-infected cells

Front 19

NK functions

Back 19

Destroys cells invaded by pathogens and also activates macrophages via IFN >> tells macrophages to upregulate MHC to facilitate destruction of ingested pathogens. granzymes and perforin mediate apoptosis of target cells.

Front 20

NK targets

Back 20

1. Markers of virally infected cells: low MHC or high MIC (surface proteins signaling stress); 2. Antibody-dependent cell-mediated cytotoxicity: Fc receptor allows binding of antibody-bound targets.

Front 21

NK surveillance

Back 21

NK's detect MHC on cell surface. MHC-1 = healthy >> inhibits NK. Lack of MHC-1 = unhealthy >> activates NK. Presence of MIC overrides MHC inhibition.
-MHC receptor = inhib; MIC = activating

Front 22

Macrophages

Back 22

long-lived phagocytes that act as first alarm. reside in tissues; role in innate and adaptive immunity.

Front 23

Macrophage life cycle

Back 23

immature monocytes leave bone marrow and migrate to tissues, where they mature

Front 24

macrophage functions

Back 24

phagocytosis; release inflammatory cytokines; use inflammatory mediators and acute phase proteins to attract neutrophils to injury site. activate T cells

Front 25

first encounter w/ bacteria

Back 25

No antibodies present, so macrophages rely on complement, TLR, etc to recognize microbe.

Front 26

FcR-mediated phagocytosis

Back 26

2nd line of defense if innate can't control response. B cells make specific antibodies that enhance phagocytosis via FcR binding.

Front 27

Endotoxic Shock

Back 27

In systemic infection, bloodborne pathogens activate macrophage at many sites >> massive cytokine secretion >> systemic vasodilation >> leakage into tissues >> low BP and septic shock. Often due to gram-neg bacteria

Front 28

Acute Phase Response

Back 28

proteins secreted by hepatocytes in response to TNF alpha and IL-1 and 6 from phagocytes. Act as opsonins or activate complement, further facilitating phagocytosis.

Front 29

Dendritic cells

Back 29

immunosurveillance

Front 30

conventional type

Back 30

In most organs and T-cell-rich lymphoid tissue. Antigen-presenting cells efficient @ priming naive T cells. Secrete IL-12 to activate NK's.

Front 31

follicular type

Back 31

Found in lymph nodes and spleen. Capture antigens via FcR and hold them for along time. stimulate B cells, help w/ long-term memory.

Front 32

plasmacytoid type

Back 32

Found in lymph nodes; secrete interferon

Front 33

Lack of innate immunity

Back 33

uncontrolled infection = death.

Front 34

lack of adaptive immunity

Back 34

show initial response but infection not fully cleared. failure to thrive.

Front 35

Response to bacteria

Back 35

inflammation initiated by macrophages in tissue >> cytokines and chemokines signal bloodborne neutrophils to enter tissue >> innate cells activate adaptive. Dendritic cells >> activate T and B cells >> B cells exit marrow, make antibodies that bind bacteria >> phagocytes can bind bacteria via FcR. T Cells go to infection site and help macrophages and neutrophils.

Front 36

Functions of complement components

Back 36

direct cell lysis, opsonization to facilitate phagocytosis, cell fragments generate inflammatory response, neutralization of viruses, clearing antibody-antigen complexes

Front 37

complement defect

Back 37

frequent infection

Front 38

early complement proteins

Back 38

alternative, lectin, classical pathways generate enzymes that catalyze production of C3b that covalently binds pathogen surface. Can later initiate formation of MAC complex.

Front 39

Alternative pathway

Back 39

Major pathway; C3 enters bloodstream from liver and small amt converted to C3a and C3b >>C3a = chemoattractant. C3b on pathogen + Factors B and D >> C3 convertase
**positive feedback, can be highly amplified

Front 40

5 factors needed for alternative pathway

Back 40

C3, factor B, factor D, Properdin, convertase

Front 41

function of C3b

Back 41

acts as opsin to facilitate phagocytosis and can further generage C5 convertase to initiate late steps of complement activation

Front 42

factor b

Back 42

binds C3b in presence of magnesium; exposes site for Factor D

Front 43

properdin

Back 43

binds C3 convertase and stabilizes it

Front 44

C3bBb

Back 44

C3 convertase activity; can create more C3b, recruit Factor B, amplifies process and can initiate late pathway.

Front 45

lectin pathway

Back 45

Mannose binding protein in serum binds bacterial surface and initiates formation of C3 convertase, same pathway as classical.

Front 46

classical pathway

Back 46

3rd pathway, antibody-mediated; antibody binds bacterial surface and initiates formation of convertase.

Front 47

complement receptor 1

Back 47

on macrophages and neutrophils; recognize C3b and facilitate attachment, phagocytosis, destruction

Front 48

Membrane attack complex

Back 48

late complement component; initiated by C5 convertase

Front 49

MAC mechanism

Back 49

Creates pore in membrane >> lysis and cell death.

Front 50

C1INH

Back 50

C1 inhibitor in serum that can inhibit onset of classical pathway and prevent needless generation of vasoactive compounds. lack of this inhibitor >> hereditary angioneurotic edema.

Front 51

C3 deficiency

Back 51

more susceptible to bacterial infection (C2 and C4 less problematic). More susceptible to autoimmune disease.

Front 52

CD59

Back 52

On the surface of human cells, prevents recruitment of C9 to MAC and formation of pore

Front 53

role of anaphylatoxins

Back 53

increase vascular permeability >> increases extravasation of antibodies and complement and migration of macrophages, neutrophils to site.

Front 54

extravasation

Back 54

activated macrophages release CDCL8 chemokine that attracts neutrophils, slowing them down. They use LFA-1 to bind ICAM on endothelium.