Glossary of I Exam I
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- pluripotent stem cell gives rise to what?
- myeloid progenitor cell and lymphoid progenitor cell
- Myeloid progenitor gives rise to what?
- myeloblast and monoblast
- lymphoid progenitor gives rise to what?
- T-cell precursor and B-cell precursor
- myeloblast gives rise to what?
- neutrophils, eosinophils, basophils
- monoblast gives rise to what?
- monocytes and dendritic cells
- "NEB": neutrophils, eosinophils, and basophils
- T-cell precursors give rise to what?
- NK cell and T lymphocytes
- B-cell precursors give rise to what?
- B-cells give rise to what?
- plasma cells
- monocytes and lymphocytes
- what cells are considered phagocytes?
- neutrophils, eosinophils, basophils, monocytes, and dendritic cells
- lymphoid cells are major cells of what system?
- where do B cells mature?
- bone marrow where they then circulate in blood, and settle in 2ndary organs
- where do T cell mature?
- thymus where they remain, circulate or reside in 2ndary lymphoid organs
- actions of NK cells
- effector cells targeting infected (bacteria or virus) and transformed (tumor) cells
- where are monocytes located? where are macrophages located?
- monocytes: blood
- what lineage are granulocytes?
- myeloid lineage
- another name for neutrophils?
- polymorphonuclear leucocytes or PMNs
- differences/similarities b/n mast cells and basophils
- basophils are in the blood
mast cells are in the tissue
both release histamine and development of allergies
basophils are from myeloid stem cells.
mast cells mature in tissue from immature precursor cells from the bone marrow and come from lymphoid stem cell
Both have surface IgE receptors
- of what lineage are dendritic cells?
- myeloid lineage
- action of dendritic cells
- present antigen to T cells
recognize PAMPs and phagocytize pathogens
respond to cytokines
Important in both innate and adapative immune response
- The majority of leukocytes are?
- neutrophils (NLMEB), which are 2x the size of RBC
- nucleus of neutrophil
- Action of eosinophil
- killing of antibody-coated parasites thru release of granule contents
- nucleus of eosinophil
- Characteristics of basophils
- dumb-bell shaped nucleus
granules obscure nucleus
least abundant WBC
structurally similar to WBC
produce histamine and heparin
nucleus has 2 lobes
- Are mast cells agranular or granular? Nucleus of mast cell?
Single light refractive nucleus
- blood form of macrophages
the deeper the invag of nucleus is = more mature
- monocyte derived tissue phagocytic cells
- kupffer, mesangial, microglia, tissue macrophage, LN/spleen monocyte, alveolar macrophage, serosa macrophage
- kupffer cells
- phagocytic cells found within blood sinus walls in LIVER
- Mesangial cells
- phagocytic cells found in KIDNEY
- phagocytic cells found in brain
- alveolar macrophage
- phagocytic cells found in LUNG
- serosa macrophage
- phagocytic cells found in GUT
- dendritic cell precursors (split off before becoming monocyte)give rise to what?
- langerhans cell in skin/mucosa
- 2 primary fxns of immune system
- 1. recognition and defense against foreign substances (non-self)
2. immunosurveillance (altered self)
- Characteristics of Innate arm
- non-specific clearing
NOT antigen specific
preformed (made all the time by BM)
- Characteristics of Adaptive arm
- specific clearing
"custom made" response-antigen dependent
inactive preformed (7-10 days activation)
- How does the innate arm interact with the adaptive arm?
- cells of innate communicate with adaptive to initiate adaptive response in the event that the innate system fails (presents antigen to adaptive)
- How does the adaptive arm interact with the innate arm?
- cytokines from acquired help to intensify innate
- what is infection?
- measurable immune response by the host
- what is disease?
- damage to the host has occured
occurs when immunocompromised
- what are the primary or central orgnas and tissue of the immune defense?
- thymus and bone marrow
- what are the fxns of the primary organs of the immune response?
- lymphocyte development, specificity (whether to be a T or B cell), and competence (able to serve the needs as that kind of cell)
- What are the secondary or peripheral organs and tissue of the immune response?
- spleen, lymphnodes, MALT, GALT, BALT
- What are the fxns of the secondary organs and tissue of the immune response?
- generating specific immune responses, maturation of lymphocytes to become effector cells (what that cell is going to do-the end stage of that cell) or memory cells (being able to repsond to a second challenge)
- mucosal associated
Waldeyer's ring (tonsils and adenoids)
- bronchus and epithelial passages of nares
- lyphoid nodules
urogenital lymphoid tissue
- where does hematopoiesis occur prior to the bone marrow?
- fetal liver until 5 month of gestation
- 2 major components of bone marrow
- hematopoeitic compartment and vascular sinuses
- describe hematopoeitic compartment of BM
- the spongy area that generates all stem cells for erythroblast formation, myeloid cell formation, and lymphoid cell formation
- Purpose of vascular sinuses in BM
- thin-walled veins that drain into central longitudinal vein. central vein exits the BM and drains into general blood circulation (this is how mature blood cells leave the bone marrow, but T-cells leave when immature to complete maturation in thymus)
- How do RBC and WBC cross the sinusoid capillaries?
- RBC: by pressure gradient
WBC:release substances than cross actively
- where is the thymus located?
- anterior mediastunum, near the base of the neck
- Name the 3 fxnl areas of the thymus
- cortex:where cells enter thymus thru bld. vssls--high cell density (rapid prolif)
medula:area of organization of most mature cells (repository-no active division)
- Describe capsule of thymus
- external collagenous capsule with extensions called trabeculae that divide the thymus into small fxnl units
- Fxn of thymus in immune system.
- selection of precursor T cells to make them capable of recognizing antigens complexed to molecules of the MHC AND to elimate self-reactive T cells
Cells migrate inward and mature as they approach the corticomedullary jxn where they enter the bloodstream
- Purpose of Hassall's corpuscles in thymus?
- site of cell destruction
- what happens to the thymus as we age?
- decrease in size
parenchyma replaced with adipocytes
- What peripheral lymphoid organs have lymphatic supply?
- Lymph nodes have BOTH afferent and efferent.
Spleen has NO lymphatics.
Unencapsulated lymphoid tissues have ONLY efferent lymphatics
- Where is the T cell rich area in the spleen?
- PALS around central arterioles located in the white pulp
- Where is the B cell rich area in the spleen?
- in the marginal zone where they aggregate into follicles with germinal centers (white pulp)
- Fxn of spleen?
- filtration of blood for pathogens and old or damaged blood cells
- Fxn of lymph nodes?
- sample lymph as it passes on its way back to the thoracic duct, continuosly monitoring the lymph for antigens or pathogens
- 3 layers of lymph nodes and what is found there?
- cortex: B cells (w/n follicles), macrophages and dendritic cells
paracortex: T cells, macrophages and dendritic cells
medulla: plasma cells
- Explain flow of lymph through node and interaction with lymphocytes.
- lymph enters through afferent lymphatics and percolates thru cortical sinusoids which deliver lymph in close proximity to post-cap venules. Lymphocytes extravasate thru venules to enter parenchyma
- Purpose of red pulp in spleen?
- red cell degradation
- Medulla in lymph node is the site of what?
- Place where plasma cells produce antibodies
- explain vasculature of lymph node?
- Each node is fed by a single lymphatic artery to arterioles to postcapillary venules to lymphatic vein
- fxn of M cells in GALT
- specialized APCs in gut that have a basolateral pocket containing lymphocytes and macrophages. They sample the antigenic contents and then leave the M cell and travel to lymphoid follicles called Peyer's patches.
- Role of dendritic cells.
- present antigen to T cells
central to adaptive response
of Myeloid lineage
primarily in tissue
- What is a receptor?
- membrane-bound glycoprotein with 3 domains: extracellular, transmembrane, and cytoplasmic
- What is a ligand?
- soluble or membrane-associated molecule that binds to a specific receptor (1:1 stoichiometry)
- what occurs when activational receptors lack intrinsic kinase activity?
- they recruit adaptor proteins with phosphorylating second systems
- Examples of rheostats.
- phosphorylation or dephos
on-off switches to regulate the protien's biologic activity
- What are the 3 main signal transduction pathways used by leukocytes in the INNATE response?
- 7 alpha-helical transmem R
Toll Like R
- What 3 ligands to 7 alpha-helical transmem R's respond to?
- 1. chemokines
2. N-formyl methionyl peptides
3. lipid mediators
- Overall result of any of the 3 ligands binding to 7 alpha-helical transmem R's?
- increase chemotaxis (migration into tissues to site of inflammation)
- what are chemokines?
- type of cytokines that provide signals for cell (WBC) migration and chemotaxis
Bound by chemokine R's
- Chemokine Receptors and how they fxn?
- work through G-proteins to activate andenylate cylase and increase intracellular Ca by activated PLCb2 leading to actin polymerization
- Explain Toll-like Receptors (PRRs) in INNATE response.
- 1. LPS (gram-neg bacteria) wants to interact with TLR
2. MD2 gives TLR4 ability to recognize LPS
3. LPS binds to CD14 (coreceptor protein) and now TLR4 can activate cells
4.ligand binding triggers dimerization TLR4s
5.dimerization recruits adapator molecules which bind with TIR domain of TLR4
6.recruit serine kinases IRAK
7.IRAK leads to release of NFkB (transcription factor)
8.NFkB enters nucleus to + transcription of cytokines
- Fxn of chemokines?
- induce and regulate leukocyte movements during inflammation
- What signalling pathway is involved in cytokine receptor signaling?
- Action of JAK/STAT pathway.
- 1. cytokine binds receptor, receptor chains dimerize
2.JAK on receptor tails phosphorylate each other, then phosphorylate tails
3.this forms docking station for STATs
4.JAKs phosphorylate STATs
5.p-STATs released, STATs form dimers
8.STATs enter nucleus to mediate transcription factors of activation genes
- Explain action of TCR
- 1. tyrosine phosphatase CD45 removes - P from kinase Fyn and Lyk therefore activating Fyn and Lyk
2. active Fyn p-lates cytoplasmic tails of CD3 complex
3.p-chain on CD3 complex forms docking site to recruit ZAP kinase
4.Lyk P and + CD3 bound ZAP
5. ZAP P-lates and + PLC
- Difference b/n TCR and BCR
- TCR uses CD3 to transduce signal.
BCR uses proteins Igalpha(CD79a) and Ig-beta (CD79b) which fxn as the signal transduction portion
BCR is a membrane-bound immunoglobulin
- TLRs are receptors for what?
- Ligands called PAMPS (pathogen associated molecular patterns)
Ex: LPS and LTA
- Where does signal transduction occur in the membrane?
- areas called lipid RAFTS (microdomains)
RAFTS are recruited by ligand binding, causing signaling molecules to be recruited and then activated
- What are the 2 pathways of apoptosis?
- intrinsic pathway (mitochondrial)
Extrinsic pathway (death-receptor initiated)
- Which pathway of apoptosis involves ligands?
- extrinsic. Intrinsic occurs by withdrawal of growh factors, hormones.
- Both pathways of apoptosis lead to what effector mechanisms?
- 1.activation of initiator caspases (cytoplasmic protease that chews cell up from inside)
2. executioner caspases
3.breakdown of cytoskeleton
5. apoptotic body which becomes a ligand for phagocytic cell receptors
*contents of cell never released
- What are cytokines?
- small, soluble hormone-like glycoproteins secreted by many cell types that INDUCE and REGULATE both INNATE and ADAPTIVE immune responses
- _____ and _____ play a central role in the development of chronic inflammation
- cytokines and chemokines
- What are the 4 different structural families of cytokines?
- hemotopoietin family, interferon family (anti-viral), chemokine family, and tumor necrosis family
- What is the most common mode of action in which a cytokine can act on its target cells?
- What is pleiotropy?
- 1 cytokine has a different effect on different target cells
- What is redundancy?
- 2 or more cytokines: same effect on same target
- What is synergy?
- the additive effect of 2 or more cytokines is more effective than the individual effects
- What is antagonism?
- the effects of 1 cytokine suppresses the effects of another
- High amts of TNF-a being secreted can lead to what?
- septic shock: blood volume decreases, fever increases, clotting factors get used up
- In low amts, what does TNF-a lead to?
- Local inflammation, neutrophil activation
- IL-2, IL-4 and IL-5 act on the same target to lead to what?
- B cell proliferation.
Example of Redundancy
- The combined effects of TNF-a and IFN-y leads to what?
- increased expression of class I MHC molecules on many cell types
Example of Synergy
- How does IFN-y antagonize the effect of IL-10?
- IL-10 inactivates macrophages, while IFN-y activates macrophages
- Action of SDF-1? R? Other name for SDF-1?
- Stromal Cell Derived Factor=CXCL12
causes progenitors to migrate from fetal liver to BM. Found in BM sinusoids
CXCL12 binds to CXCR4
- What cytokines are reqd for differentiation of HSC into lymphoid lineage?
- IL-3 and IL-7
- What cytokines are reqd for differentiation of HSC into myeloid lineage?
- IL-3 and GM-CSF
- IFN-y secreted by NK cells does what?
- activates macrophages
- IL-12, secreted by macrophages, does what?
- stimulates NK cells to secrete more IFN-y
- What complement split products bind R's on mast cells and cause degranulation?
- C3a and C5a
- What are the 3 cytokines involved in extravasation?
- IL-6, IL-8 and TNF-a
Primary action of IL-8
- What are the 4 steps of extravasation?
- rolling, tethering(integrin activation by chemokines), tight binding, diapedesis(migration through endothelium)
- What cytokines induce the acute phase response in innate immunity?
- IL-1, IL-6 and TNF-a
They tell hypothalamus to release prostaglandins and induce fever.
Tell liver to release acute phase proteins.
Tell BM to increase WBCs
- What effect does TNF-a have on endothelial cells?
- express adhesion molecules (selectins and integrins)
- What effect does TNF-a have on smooth muscle cells?
- increase blood flow to venules to increase vascular permeability
- Type I interferons?
Type II interferons?
- Type I: IFN-a and IFN-b
Type II: IFN-y
- Effect of Type I Interferons on uninfected cells?
- induce production of antiviral proteins to block viral replication
- Effect of Type I interferons on virus infected cells?
- increased expression of MHC I molecules on infected cells, which leads to killing by Tc
- What produces IFN-a? IFN-b?
- IFN-a: macrophages, monocytes, lymphocytes
IFN-b:fibroblasts, epithelial cells
- What produces IFN-y?
- T cells, NK cells
- Roles of IFN-y?
- macrophage activation
T cell differentiation
- What are IPCs or plasmacytoid dendritic cells (pDC's)
- cells that produce IFN-a and b w/n the first 4 hours of a viral infxn. Their specialty is to produce large amts of Type I IFNs upone viral stiumulation
- what type of R's do IPC's express?
- TLR-7 and TLR-9 (intracellular)
- What does a pDC do upon detecting a foreign agent?
- increase expresion of MHC proteins and secrete pro-inflammatory cytokines
- How do DC's that swallow viruses respond?
- secrete Type I IFNs and cytokines IL-2 and IL-12 which act to bind to R's on NK cells causing NKs to secrete IFN-y (Type II IFN) and enhance production of granzymes and perforin
- What are 2 cytokines that resolve the acute inflammatory response?
- IL-10 turns off transcription of TNF-a genes (cytokine syn inhibiting factor) ANTI-INFLAMMATORY
TGF-b:begins wound healing
- Name 2 cytokines in chronic inflammation that are continuosly produced.
Involved in maintenance and expansion of a granuloma-body's way of walling off infxn
- Name the endogenous pyrogen cytokines.
- IL-1, IL-6 and TNF-a
- Action of IL-1
- produced by APC's, T, Bs
acts to induce acute phase response by increasing expression of adhesion molecules, induce fever, acts on T cells
- Action of IL-6
- regulate acute phase response, regulate inflammation
- Action of IL-12
- secreted by macrophages
stimulates NK cells to secrete more IFN-y and produce more perforins and granzymes
- Action of chemokines
- cytokines that provide their target cells signals for extravasation and chemotaxis (direct T cells from BM to thymus)
- Action of IL-8.
- neutrophil extravasation and chemotaxis in an accute inflammatory response
- Action of IL-2
- main autocrine cytokine that stimulates GROWTH of T cells, B cells, NK cells, monocytes, and macrophages
- Action of IL-4
- Paracrine cytokine
secreted by T cells and mast cells
stimulates B cells to isotype switch
- cytokines involved in humoral immune response
- IL-4 and IL-5
- Which cytokine stimulates growth and differentiation of eosinophils?
- What 2 cytokines inhibit macrophage activation?
- IL-10 and IL-4
- Main action of IL-10?
- anti-inflammatory (inhibits cytokine synthesis)
- Name 2 cytokines involved in the humoral mediated immune response.
- IL-4 and IL-5
- What cytokine is the major player in activating the cell-mediated arm of the adaptive immune response?
- IFN-y by inhibiting production of IL-4 and IL-5 therefore inhibiting a humoral adaptive immune respone
- Which cytokine stimulates the proliferation of T cells in an autocrine fashion, once the TCR is bound?
- Besides being anti-inflammatory, what else does IL-10 do?
- inhibits development of cell-mediated immune responses...favors HUMORAL ADAPTIVE response
- Under the influence of IL-12, a naive T cell becomes what?
- TH1 cell for CELL-MEDIATED adaptive response
- Under the influence of IL-4, a naive T cell becomes what?
- TH2 cell for HUMORAL ADAPTIVE immune response
- Major fxns of the innate system
- 1. identification and removal of foreign substances
2. recruitment of immune cells
3.activation of the complement cascade
4.activation of the adaptive immune system through antigen presentation
- What is the 1st line of defense of the innate system?
- mechanical and physical effectors: skin, cilia, sneezing
chemical effectors: body secretions, complement
- What is the 2nd line of defense of the innate system?
- phagocytic cells
- What are some examples of mechanical effectors of our 1st line of defense?
- intact skin (desquamation to remove pathogens), cilia to move out what we inhale, sneezing, urinating, vomiting
- What are some examples of chemical effectors of our 1st line of defense?
- organic acids, inorganic acids (HCL in stomach), hydrolytic enzymes (lyzozymes in tears), surfactants, defensens produced by surface GI tract
- What is the biological effector of our 1st line of defense?
- commensal flora: exhibit competitive exclusion by populating surface of GI making it difficult for bacteria to enter, secrete anti-microbials and have PAMPS on surface
CONSTANT stimulus of immune system
- What are the humoral barriers to infxn of the INNATE?
- coagulation system
- How does coagulation help initiate complement?
- coagulation bi-products (plasmin)stimulate complement
- Name 3 ways in which complement can be activated?
- -specific PAMPs
-elements of clotting cascade
-presence of antibodies
- Primary fxn of complement?
- -killing via MAC or phagocytosis
-generation of anaphylatoxins
- What is the job of NK cells and how do they do it?
- kill damaged or altered "self" cells forming pores via perforins, and secrteting granzymes leading to apoptosis
- Name the cells of the innate system?
- NK cells (lymphoid lineage)
all cells of myeloid lineage
- What receptors are found on NK cells?
- KAR: killer activating
KIR: killer inhibiting
- What ligands are on target cells that NK cells attack?
- KAL: killer activating
ex: viral antigens or tumor antigens "stress proteins"
- What does the KIR on NK cells bind to?
- MHC I on non-virally infected cells
- What are the 2 pathways in which cell death via lysis will resulte from NK activity?
- peforin pore created and granyzmes entering OR
FAS ligand binding to FAS R
- Which cells are considered NON-PHAGOCYTIC cells?
- mast cells (release histamine from granules), basophils (release histamine ), eosinophils (secrete highly toxic proteins effective against bacteria and parasites..but causes tissue damage)
- Are dendritic cells central to the innate or adaptive immune response?
- What are the phagocytic cells of the INNATE?
- Features of neutrophil granules?
- 2 types of antimicrobial cytoplasmic granules:
1. primary or azurophilic granules
2. secondary granules
- Which of the phagocytic cells are granular?
- neutrophils NOT monocytes
- When do monocytes become macrophages?
- mono: blood
- Although macrophages donot contain granules, what do they contain?
- lysosome - vesicles in cytoplasm
- How are phagocytic cells recruited?
- via PRR's (Pattern recognition receptors)located on surface of immune cells to recognize PAMPs
ex: TLR, complement receptors, mannose receptors
- Where are PAMPs located?
- on surface of microbes or microbial products
ex: LPS, Glycolipids, N-Formyl peptides (evidence of prokaryotic proteins)
- How does phagocytosis work?
- recognition of foreign cell via PRRs, bacteria endocytosed, form phagosome, lysosome merges with phagosome to form phagolysosome, degradation by lysosomal contents, exocytosis of degraded parts
- Explain the oxidative Dependent-respiratory burst used by phagocytes to kill.
- 1.NADPH oxidase reduces O2 to superoxide
2. superoxide dismutase then converts it to H2O2
3.Myeloperoxidase uses superoxide and chloride ions to produce hypochlorous acid
- Oxygen INDEPENDENT mechanism of phagocytic killing?
- ex: preformed lactoferrin, cathepsin D
- 3 killing mechanisms of phagocytes?
nitric oxide dependent
- explain nitric oxide dependent killing used by phagocytes.
- IFN-y and TNF bind and stimulate NO sythetase enzyme to convert O2 and arginine to NO and citrulline
- What is complement and what is the function?
- C' refers to a group of 20 proteins which act together to
1. Opsonize antigen
2.enhance inflammatory response
3. lyse microorganisms
- Overproduction of cytokines can cause what?
- tissue damage during chronic inflammatory rxns
- What is C'-fixation?
- utilization of C' by Ag-Ab complexes
- How is a complement cascade initiated?
- some complements act as pro-enzymes that are activated by cleavage and when activated cleave one or more complement proteins
- Which C' pathway is the primary pathway of the innate system?
- What is the importance of C3 convertase?
- producing more C3b for opsonizing bacteria
- How is the classical C' pathway initiated?
- by binding of Ag-Ab complex
- How is the alternative pathway initiated?
- By pathogen surfaces. Tick Over: spontaneous activation of C3 in the presence of water
HIGHLY regulated step in that if it is not inactivated C3 amts would diminish in our body. Once activated C3 binds to antigen
- What is the importance of the C5 convertase?
- form MAC complex-support
- Which pathway is part of the innate humoral response?
- alternative therefore it is NONSPECIFIC
- Fxnl activation of the alternative pathway is via interaction with specific molecules on the surface of microorganisms in the absence of antibody. Name some examples.
- Complex polysaccharides: mannose
Lipoligosaccharides: E coli
- In the alternative pathway, what Factor cleaves Factor B?
- Factor D
- In the alternative pathway, what makes up the C3 convertase?
- What does Factor H do to the C3 convertase? Properdin?
- binds and dissociates it
P: binds and stabilizes it
- What is the C5 convertase of the alternative pathway?
- Action of Factor I?
- C3b inactivator (all pathways)
- What initiates the membrane attack complex formation?
- formation of C5 convertase
- What is a MAC?
- transmembrane pore in the target cell resulting in leakage of the cytoplasmic contents
- Which types of target cells are resistant to MAC?
- encapsulated bacteria
gram positive bacteria
- Which complement pathway is part of the adaptive humoral response?
- clasical..very SPECIFIC
- What immmunoglobins activate the classical C' pathway?
- Ig-M *best activator b/c polymeric
Ig-G- not as good b/c need high density to elicit activation
- What is the structure of C1?
- 3 protein subunits: C1q, C1r, C1s
- What is the action of C1q? C1r? C1s?
- C1q: bind Fc region on Ab causing figure 8 conf. change in C1r and C1s
C1s: cleaves C4 and C2
- C3 convertase of classical and lectin pathways?
- C5 convertase of classical and lectin pathways?
- Is the lectin pathway part of innate humoral or adaptive humoral?
- innate humoral...non specific in that it binds to conserved ligands on the surface of microorganisms
- How is the lectin pathway initiated?
- MBL binds to mannose or N-acetylglucosamine R's on microorganisms (mannose is only found on pathogens..not on our cells)
- Lectin pathway after MBL binds?
- stimulates MASPs to cleave C4 and C2
- What are the regulatory components of the classical and lectin pathways?
- C1-INH, C4-BP, Factor I
- Which complement proteins participate in opsonization?
- C3b, C4b and iC3b
- What do C3b and C4b opsonize?
- proteins and carbs on surfaces of microorganisms
- what does iC3b opsonize?
- immune complexes. attaches Ag-Ab complexes to RBC which drop off complexes in the liver and spleen for removal
- What cleaves C3b into iC3b?
- Factor I
- Which complement components act as anaphylatoxins?
- C3a and C5a
mediate degran of mast cells, basophils/chemotaxis/promote smooth muscle contraction
*C5a also increases expression of C' R's
- Which C' components participate in lysis?
- How does C3b neutralize microorganisms?
- by binding to the surface of viruses blocking the ability of the microbes to adhere, thus blocking the disease process
- Activity of C2b fragment?
- prokinin resulting in edema
- What is the most potent anaphylatoxin split C' product?
- What is the least potent anaphylatoxin split C' product?
- Control factor for C5b67 fragment? Result?
- Protein S (vitronectin)
- A deficiency of C3 could lead to what disease?
lack opsonization and inability to utilize MAC pathway
- Deficiency of Factors H or I could lead to what?
- uncontrolled activation of C3 via alternative pathway resulting in depletion of C3
- Deficiency of C1-INH would lead to what?
- hereditary angioedema due to overproduction of C2b(prokinin)
- Purpose of C1-INH?
- blocks C1rs from cleaving C4 and C2 b/c too much C2b can cause edema
-downregulates the activity of the classical pathway of C', the coagulation cascade, and the kinin
- What is an example of a non-immune initiator of inflammation? immune?
- non: trauma
immune: infectious agents
- Purpose of acute inflammation?
- delivers plasma and cellular components of the blood to tissue spaces for clearing and repair
- When does chronic inflammation occur?
- when the acute response is not adequate to clear the tissue leading to granuloma formation
- cellular players in acute inflammation?
- mast cell, neutrophil, macrophages
- action of histamine in inflammation?
- increase vaso perm, vasodilation
- action of prostaglandins in inflammation?
- vasodilation, edema
- action of leukotrienes in inflammation?
- Action of neutrophil primary granules?
- microbial killing and digestion
- action of neutrophil secondary granules?
- increased expression of CAMs on neutrophils is due to what?
on endothelial cells?
- neutrophils: thrombin release from platelets
- roles of selectins, integrins and CAMs in extravasation process?
- selectins: rolling adhesion
integrins: firm adhesion
- 1st cell to participate in inflammatory response?
- neutrophils (degranulation) then macrophages (phagocytosis) low in # before inflammation begins
- role of platelets in inflammation?
- produce chemotactic factors for PMNs
produe oxygen radicals contributing to tissue damage
block damaged vessel walls to prevent hemorrhage
- 5 cardinal signs of inflammation
- rubor: redness
tumor: swelling (vasoperm)
calor: heat (vasodilation)
dolor: pain (prostaglandins)
functio laesa: loss of fxn
- Immediate effect of inflammation?
- white line of VASOCONSTRICTION
- 3-50 seconds into inflammation?
- redness due to vasodilation of capillaries
- 30-60 seconds into inflammation?
- increased flush due to vasodilation of arterioles
- 1-5 minutes into inflammation?
- wheal formation due to increased vascular permeability
- After the initiation, what happens next in inflammation?
- neurologic vasoconstriction due to syphathetic NS
- After neurologic vasoconstriction, what occurs next in inflammation?
- acute vascular phase: release of vasoactive cmpds from mast cells and macrophages leading to endothelial cell contraction (vasodilation) and transudate release
- If inflammation is due to a nonimmune stimulus, where does it stop?
- after acute vascular phase
- What step occurs after acute vascular phase in inflammation?
- acute cellular phase: chemotaxis, margination and emigration of neutrophils; diapedesis of RBCs
- at what stage of the inflammatory response can you reach resolution if the stimulus is adequately removed?
- after acute cellular phase
- What happens in the chronic cellular phase?
- emigration of lymphocytes, infiltration by macrophage, emigration of eosinophils in parasitic infxns or in allergic responses
- Purpose of the acute phase response?
- heterogenous group of serum proteins that increase during inflammation and serve to replace exhausted components, reinforce innate defenses against infxn, limit damage, or increase the inflammation
- Name some representative components of the acute phase response.
- CRP- C reactive peptide
SAA-serum amyloid A protein
- What cytokines trigger the acute phase response?
- IL-1, IL-6, TNF-a
- When might chronic inflammation occur?
- if tissue damage is extensive or if the initiating stimulus persists
- What might chronic inflammation result in?
- granuloma formation
significant tissue damage
compromise of normal fxn
- What is the major immune cell in chronic inflammation?
- lymphocytes (t cells)
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