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162 Cards in this Set
- Front
- Back
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Hematopoietic stem cell derivatives (WRT immuno)
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common lymphoid progenitor
common myeloid progenitor |
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Common Lymphoid Progenitor derivatives...
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1. B cell ---> Plasma Cell
2. NK/T cell precursor ... gives rise to... a) T cell ---> effector T cell b) NK cell |
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common myeloid progenitor derivatives:
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1. common Granulocyte precursor:
a) N.E.B. 2. "unknown precursor" a) mast cell b) monocyte i) macrophage ii) dendritic cell |
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Granulocytes
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NEB!
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mast cell origin:
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common myeloid progenitor
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monocyte derivatives
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dendritic cell
macrophage |
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Primary lymphoid Tissues
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Bone Marrow - B cell maturation
Thymus - T cell differentiation. |
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Secondary lymphoid Tissues
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WHERE RESPONSE IS STARTED, not where the cells came from:
Spleen MALT Lymph Nodes |
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Innate Response
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Non-specific/indiscriminate
PRRs to ID GENERAL CLASSES of pathogens by binding to PAMPs (pathogen associated molecular patterns). |
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Adaptive Response general def.
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specific and focused
ANTIGENIC FRAGMENTS presented on specialized molecules (MHC) to cells to ID pathogen |
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Adaptive immunity forms:
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Humoral
Cell mediated |
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Humoral immunity
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mediated by Ab that are produced by B CELLS.
EXTRACELLULAR PATHOGENS. |
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Cell-mediated immunity - responsible cell and process
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T CELLS
TCR is T cell antigen recognition receptor (similar to Ab molecule). Useful against INTRACELLULAR pathogens. |
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mediated by Ab that are produced by B CELLS.
EXTRACELLULAR PATHOGENS. |
Humoral immunity
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T CELLS
TCR is T cell antigen recognition receptor (similar to Ab molecule). Useful against INTRACELLULAR pathogens. |
Cell-mediated immunity
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T cell receptor vs. Ab molecule
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T cell receptor is NEVER SECRETED. It's always membrane bound.
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4 major points WRT innate immunity:
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Rapid response (hours)
Fixed Limited number of specificity constant during response. |
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4 major points WRT adaptive immunity
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slow response (days-weeks)
Variable numerous highly selective specificities improve during response. |
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Lymphocytes --> abundance and makeup...
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35% of total WBC population
Includes B cells and T cells |
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35% of total WBC population
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Lymphocytes
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B Cells
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lymphocyte
develop in bone marrow produce Ab (5 classes) --> IgM, IgD, IgA, IgG, IgE |
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produce Ab (5 classes) --> IgM, IgD, IgA, IgG, IgE
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B cells
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T cells and examples
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lymphocyte
originate in bone marrow, differentiate/develop on THYMUS. CD4+ and CD8+ |
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CD4+
what does it do? |
T helper cell.
provide regulatory signals to both B cells and CD8+ cells Activate macrophages. Includes Treg and maybe others... |
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T helper cell.
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CD4+
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CD8+
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Cytotoxic T cells
kills virally infected cells and cells displaying foreign antigens. |
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Cytotoxic T cells
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CD8+
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NK Cells
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Lymphocyte
Large, granular. Don't produce Ab or display TCR. Kill virally infected cells and tumor cells. |
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Neutrophil
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granulocyte
aka PMNs most abundant WBC phagocytosis. express PRRs |
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granulocyte
aka PMNs most abundant WBC phagocytosis. express PRRs |
Neutrophil
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Eosinophils: percent, action...
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2-5% of WBC population
NOT PHAGOCYTIC. parasite infection elim. express receptors for IgE and present at sites for IgE mediated allergic rxns. |
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2-5% of WBC population
NOT PHAGOCYTIC. parasite infection elim. express receptors for IgE and present at sites for IgE mediated allergic rxns. |
Eosinophils
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Basophils + percent abundance??
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1 percent WBC population.
NOT PHAGOCYTIC expresss high affin for IgE FcR(E). Binding of IgE to receptor induces histamine release from basic staining granules. |
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1 percent WBC population.
NOT PHAGOCYTIC expresss high affin for IgE FcR(E). |
Basophils
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Mast Cells
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PRIMARY CELL IN ALLERGIC RESPONSE.
resident in all CONNECTIVE TISSUES. express FcR(E). Upon binding IgE they release histamine etc. |
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PRIMARY CELL IN ALLERGIC RESPONSE.
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Mast cells
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Monocytes - percentage abundance; development, etc...
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4% of WBC population
Develop in bone marrow; migrate to tissues and mature into macrophages (Mo). Phagocytic (highly) APCs to lymphocytes. involved in both innate and acquired immune responses. principal cells invovled in inflammatory response (produce IL1, TNF, and IL6). |
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Monocyte types/why...
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differentiated based on what tissue they're in:
Microglial cells -CNS Kupffer cells - Liver Alveolar Macrophages - pulmonary airways osteoclasts - bone |
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Microglial cells -CNS
Kupffer cells - Liver Alveolar Macrophages - pulmonary airways osteoclasts - bone all types of what cell?? |
monocytes.
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IL1, TNF, and IL6 from where?
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monocytes.
inflam repsonse. |
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dendritic cells
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high APC function.
2 types: 1. Interdigitating 2. follicular |
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interdigitating DCs
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T cell rich areas of lymphoid tissues; pick up Ag and migrate to draining node to present Ag to T cells.
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present Ag to T cells.
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interdigitating DCs
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follicular DC
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follicles of nodes and spleen
present Ag to B cells. |
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present Ag to B cells.
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follicular DC
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Thymus + structure!
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Site of T cell diff.
1. Cortex: thymocytes, (immature T lymphocytes), and cortical epi cells which "nurse" T cell development. 2. Medulla: functionally mature T cells. |
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first organ of immune system to form (6-8 wks).
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Thymus
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Lymph Nodes
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filter lymph drawn from tissues/local infections.
1. Cortex: B cells and macrophages in primary follicles. Many will develop into GCs upon Ag stim. 2. Paracortex: btw cortex and medulla --> T cells and Interdigitating DCs 3. Medulla: lymphocytes leaving via efferent lymphatics. |
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Spleen
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Filters blood... SYSTEMIC INFECTIONS.
1. Red pulp --> sinusoids populated by macrophages and RBCs. 2. White pulp: lymphoid cells: a) T cells sit in PALs (cuffs of lymphoid tissues that surroound small arterioles). b) B cells: follicles outside the PALs. c) marginal zone: rim of B cells and macrophages. |
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MALT includes... and MALT "types"...
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tonsils, adenoids, appendix, Peyer's patches.
GALT BALT NALT VALT (vulvovaginal assoc. lymphatic) |
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MALT structure:
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follicles interspersed with T dependent areas.
NO MEDULLA. pathogens delivered across mucosa by M CELLS (specialized epi cells). |
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M CELLS
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specialized epi cells
deliver pathogens across mucosa in MALT. |
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Extravasation
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mvt of cells from blood into tissues.
includes homing and diapedesis. |
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mvt of cells from blood into tissues.
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Extravasation
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Homing + 4 players
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directed mvt of cells via interaction of surface adhesion molecules:
1. integrins 2. selectins. 3. mucin-like CAMS/Addressins 4. Immunoglobulin superfamily CAMs. |
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Integrins
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Heterodimers with alpha and beta chains.
3 familes determine what beta chain: 1. beta1 --> binding cells to EC matrix (VLA1-VLA6). 2. beta3 --> platelet/neutro interaction at vasc damage sites. |
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Heterodimers with alpha and beta chains.
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Integrins
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Selectins
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expresssed on:
1. leukocytes (L-selectin) 2. activated endothelial cells (E-selectin). 3. platelets (P-selectins). Lectin-like specificity for sugars expressed on HEAVILY GLYCOSYLATED MB PROTEINS. binding slows down circ. leukocytes w/i venules. |
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specificity for sugars expressed on HEAVILY GLYCOSYLATED MB PROTEINS.
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Selectins
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Mucin-like CAMS/Addressins + examples(2)
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expressed on HEVs.
--> bind circulating T cells and direct them to lymphoid tissue. Heavily glycosylated serine/thr rich ex= CD34 and GlyCAM-1 |
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HEVs WRT addressins:
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HEVs of diff. tissues have different sets of adhesion molecules giving them distinct "address."
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CD34 and GlyCAM-1
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Mucin-like CAMS/Addressins
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Ig superfamily cell adhesion molecules + examples (3)
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families of molecules which contain at least on Ig domain.
ex: 1.ICAM-1,2,3. 2.VCAM (on vascular endothelial cells) 3.MAdCAM-1 |
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MAdCAM-1
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both Ig and mucin like domains expressed by mucosal endo cells.
directs lymphocytes into mucosa. binds to integrins via Ig-like domain and to selectins via mucin-like domain. |
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both Ig and mucin like domains expressed by mucosal endo cells.
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MAdCAM-1
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Diapedesis
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type of extravasation
migration through endo cell barrier. |
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Barriers to infection
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part of innate immune response.
mechanical, chemical, and microbiological. |
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Examples of mechanical barriers:
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epithelial cells joined by tight junctions (all over).
longitudinal flow of air or fluid (skin and gut). movmement of mucus by cilia (lungs). |
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Chemical barriers to infection and examples (2).
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inhibit attachment and growth of microbes.
1. lysozyme -- found in tears, saliva, mucus, and blood. Degrades bacterial cell walls. 2. acid and hydrolases (stomach). |
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degrades bacterial cell walls
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lysozyme
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microbiological barriers
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normal flora (in skin and gut) compete with pathogens for food and a place to live.
extra --> recall antibiotics/eating yogurt. |
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5 Stages of infection:
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1.pathogen adherence to epithelium
2.penetration of epithelium. 3.local infection (innate response) (extracellular vs intracellular). 4.lymphatic spread 5.activation of adaptive immune response. |
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extracellular local infection
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located on
1. interstitium (e.g. viruses, bact, protozoa) 2.epi surfaces |
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intracellular local infections
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1. cytoplasmic --> e.g. viruses.
-fight with NK cells. 2. vesicular --> e.g. mycobacteria. -fight with activated macrophages. |
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Innate immune response defenses:
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1. non-cellular
a) complement b)defensins c) lysozyme. 2. cellular defenses a)macrophages b)neutrophils c)NK cells. |
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Complement --> what type of defense is it?
deficiency=? regulation? component production/function? |
noncellular/extracellular INNATE immunity.
recurrent infections regulated by soluble factors and surface bound molecules. component prod. constitutively by liver and coat surface of bacteria and extracellular viruses. |
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complement pathways:
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1. alternative pathway --> pathogen surface creates envt. conducive to complement activation. FIRST TO ACT.
2. Lectin pathways --> mannose-binding lectin binds to pathogen surface. SECOND TO ACT. 3. Classical pathway --> C-reactive protein or antibody binds to specific antigen on path. surface. THIRD TO ACT. |
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complement activation via 3 paths results in??
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cleavage of C3 to C3a and C3b, with C3b COVALENTLY BOUND TO SURFACE OF PATHOGEN.
results in: 1. recruit inflam. cells. 2. opsonization of phatogens (facilitates uptake/killing by phagos). 3. perforation of pathogen cell membranes 1-3 = death of pathogen. |
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3 complement pathways merge at?
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C3 cleavage to a and b.
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What does complement path terminate in?
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formation of MAC (mb attack complex).
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C3b
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complement cascade; at cleavage of C3... remains attached to pathogen.
targets/marks pathogen for destruction. |
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Alternative pathway WRT complement (general/overall schematic).
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1. C3 spontaneous hydrolysis --> iC3. CATALYZED BY PROXIMITY OF BACTERIA.
2. iC3 picks up B. Then picks up D. --> iC3Bb (equals SOLUBLE C3 CONVERTASE). 3. soluble C3 convertase cleaves C3 into C3a and C3b. 4. C3b binds to microbe surface 5. C3b picks up factor B and then D. --> ALTERNATIVE C3 CONVERTASE. 6. C3bBb cleaves C3 into C3a and C3b. results in positive feedback loop for C3b deposition and additional C3 convertase formation. 7. C3b binds to alternative C3 convertase forming alternative C5 convertase (C3b2Bb) |
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Alternative pathway (complement) allows for?
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AMPLIFICATION OF SIGNAL.
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General regulation WRT complement control:
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1. plasma proteins (recall from liver) --> interact with C3b attached to human and microbial cell surfaces.
2. mb proteins-->prevent complement fixation on human cell surfaces. |
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Properdin (factor P)
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plasma protein involved in control of complement cascade.
stabalizes formation of AltC3 convertase allowing for large depostions of C3b. |
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stabalizes formation of AltC3 convertase allowing for large depostions of C3b.
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Properdin (factor P)
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Factor H
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plasma protein WRT compelement control.
binds C3b and allows for interaction with Factor I. Factor I cleaves C3b into iC3b, which can't function as a convertase. e.g. allows downreg. of complement reaction. |
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plasma protein that allows downreg. of complement reaction
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factor H.
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Decay Accelerating Factor (DAF)
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membrane prot WRT complement regulation/control.
binds C3b and C3bBb causing C3b to dissociate and inactivate C3b in HUMAN CELL SURFACES. regulates C3b deposition; helps immune system distinguish self vs non-self. |
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Factor I deficiency
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leads to depletion of C3 because unchecked regulation of C3bBb formation.
more susceptible to infections with encapsulated bacteria. |
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binds C3b and C3bBb causing C3b to dissociate and inactivate C3b in HUMAN CELL SURFACES.
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DAF
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Membrane cofactor protein
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membrane protein wrt complement control.
similar to DAF; also allows for factor I to bind and cleave C3b into iC3b. involved at HUMAN CELL SURFACE. |
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Receptors involved in "Alternate Pathway" of complement.
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CR1, CR2, CR3, CR4...
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CR1
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complement receptor; alternative pathway.
binds C3b. facilitates phagocytosis of bacteria. protects human cells form complement functioning like MCP and factor H by making C3b susceptible to inactivation by factor I. |
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protects human cells form complement functioning like MCP and factor H by making C3b susceptible to inactivation by factor I.
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CR1
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CR3 and CR4
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complement receptor; alternative pathway.
bind iC3b, facilitates phagocytosis of bacteria. |
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C3b2Bb formation and function:
what is it called? |
C3b + C3bBb (alt C3 convertase) --> C3b2Bb.
cleaves C5 into C5a and C5b. C5 convertase |
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cleaves C5 into C5a and C5b.
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C3b2Bb = Alt C5 convertase.
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C5b pathway to formation of MAC/completion of pore:
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assocates with C6 and C7.
MAC attaches to microbe surface. C8 binds to MAC and allows for binding and polymerization of C9. Polymerization = pores. |
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C9 polymerization info:
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10-16 C9 per C5-8.
Pore formation = osmotic lysis. |
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Plasma proteins that regulate/inhibit MAC and what they do:
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S protein
Clusterin Factor J All prevent C5b67 from attaching to cell surface. |
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membrane proteins that regulate MAC and how they work:
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homologous restriction factor
CD59 prevent recruitment of C9. |
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homologous restriction and factor
CD59: structure and function |
membrane proteins.
prevent recruitment of C9. |
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S protein
Clusterin Factor J Structure and function |
plasma proteins
All prevent C5b67 from attaching to cell surface. |
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C3a and C5a functional name:
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Anaphylatoxins
increase inflamation at site of Complement activation --> "allergic-like activity" |
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Anaphylatoxins
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C3a and C5a.
increase inflamation at site of Complement activation --> "allergic-like activity" induce smooth muscle contraction and degranulation of mast cells and basophils = HISTAMINE RELEASE = vascular perm. increase. |
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C5a
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most stable and potent anaphlotoxin.
chemoattractant for neutrophils and monocytes (toward site of complement activation). |
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Name 4 noncellular/extracellular defense systems other than complement and how they do it:
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1.coagulation: immobilize microorgs.
2.defensins: anti-microbial peptides that penetrate and disrupt integrity of microbe cell membranes. *functionally limited to sweat, tears, gut lumen, or phagosomes. 3. protease inhibitors: counteract pathogen derived proteases 4. lysozyme: degrades bacterial cell walls; found in saliva, tears; secreted by paneth cells; packaged within neutrophil granules. |
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lysozyme - what does it do? where do we see it? What secretes it and where is it packaged (2)
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degrades bacterial cell walls
found in saliva, tears secreted by paneth cells; packaged within neutrophil granules. |
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degrades bacterial cell walls; found in saliva, tears; secreted by paneth cells; packaged within neutrophil granules.
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lysozyme
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anti-microbial peptides that penetrate and disrupt integrity of microbe cell membranes. *functionally limited to sweat, tears, gut lumen, or phagosomes.
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defensins
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defensins
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anti-microbial peptides that penetrate and disrupt integrity of microbe cell membranes. *functionally limited to sweat, tears, gut lumen, or phagosomes.
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phagocytic receptors + why do they work?
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bind bacterial components aiding in phagocytosis.
work because carbs of microbes have stuff not present in euk. cells, making them target for receptors on innate immune cells. PRRs and PAMPs |
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Lectins + 2 examples
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receptors and plasma proteins that recognize carbs.
ex= mannose and glucan receptors. |
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scavenger receptor
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binds assortment of ligands that are NEGATIVELY CHARGED.
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Mannose receptor and Glucan receptors bind what? what are they?
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Lectins
phagocytic receptors |
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CR3 and CR4 - what type of receptors are they? What do they do?
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phagocytic receptors
bind iC3b and LPS |
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LPS significance:
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in the outer membrane of gram negative bacteria.
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gram positive vs gram negative
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gram positive --> petidoglycan outside... holds stain.
gram negative --> peptidoglycan wall surrounded by OUTER MEMBRANE (w/ LPS). doesn't hold dye. |
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phagocytosis: cellular players + process example
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neutrophils and macrophages
example: 1. complement activation; C3b deposited on surface of bacteria. 2. CR1 on macrophage binds C3b on bacteria. 3. endocytosis by macrophage, creates vessicle with bact. inside called PHAGOSOME. 4. Lysozomes fuse with phagosomes --> PHAGOLYSOZOME. |
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Signaling receptors + what happens when they're bound:
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on cells of immune system.
bind bacterial ligands (PAMPs) that are distinct from human cells. **Can bind directly to motifs, OR to HOST plasma proteins that bind specific bacterial components. Binding of receptor initiates cascades yielding CYTOKINES --> recruit other immune cells. |
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TLRs
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Major innate signaling receptors.
Detect all kinds of stuff, from gram pos. and neg. bact, to viruses etc etc. necessary for INNATE IMMUNE RESPONSE BUT ALSO sets stage for ADAPTIVE response, if needed. |
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Major innate signaling receptors.
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TLRs
(Toll-like receptors). |
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Function of TLR relates to what?
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Cellular location.
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TLRs that recognize extracell. microbes?
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1,2,4,5,6
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TLRs that recognize microbes in endosomes??
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3,7,8,9.
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TLR5 recognizes what?
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Flagellin
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Flagellin recognized by what TLR?
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TLR5
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TLR4 recognizes what?
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LPS
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LPS recognized by what TLR?
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TLR4
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TLR3 recognizes what?
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dsRNA
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dsRNA recognized by what TLR?
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TLR3.
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TLR7 and TLR8 recognize what?
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ssRNA
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ssRNA recognized by what TLR(s)?
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7 and 8
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TLR9 recognizes what?
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CpG DNA
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CpGDNA recognized by what TLR?
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9
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TLRs WRT microbial recognition. what happens?
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TLR2 forms heterophilic dimer with TLR1 or TLR6.
Others form homodimers. |
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MyD88
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adapter protein common to all TLRs except TLR3
involves NF-kappaB activation, which leads to SYNTH. AND SEC. OF TNF-alpha and other cytokines. |
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involves NF-kappaB activation.
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MyD88
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TLR3 utilizes what pathway?
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IRF3 activation leading to production of type I Interferon (alpha and beta).
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TLR4 is unique because?
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it can utilize both pathways:
Type I interferons via IRF3 TNFalpha etc. via NFkappaB. |
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4 examples of cytokines we talkeda about:
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TNF
Interleukin 1(IL-1) IL-6 Chemokines |
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IL-6
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systemic: Fever, Acute phase protein production by hepatocytes.
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systemic: Fever, Acute phase protein production by hepatocytes.
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IL-6
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TNF-alpha
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local effects: increases vasc. permeability.
systemic: fever, shock etc. |
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local effects: increases vasc. permeability.
systemic: fever, shock etc. |
TNF-alpha
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IL-1
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Local: activates lymphocytes, activates vasc endo.
Systemic: Fever, production of IL6. |
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Local: activates lymphocytes, activates vasc endo.
Systemic: Fever, production of IL6. |
IL-1
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IL12
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activates NK cells.
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activates NK cells.
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IL12
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steps in extravasation/cellular recruitment:
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rolling adhesion
tight binding diapedesis migration |
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Respiratory Burst + protection.
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production of toxic oxygen radicals and H2O2 via NADPH oxidase in Neutrophils.
Protect host via: superoxide dismutase catalase (H2O2 --> H2O+O2) |
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acute phase response + examples
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occurs via bacteria inducing macrophages to prod. IL6, which acts on hepatocytes to induce synth of acute phase proteins:
1. C reactive protein 2. Mannose binding lectin. |
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Mannose binding lectin
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binds to mannose containing carbs on bacteria, viruses, etc...
Can activate COMPLIMENT CASCADE: 1. MBL binds C2 and C4, cleaving them into C2a, C2b, C4a, and C4b. 2. C2a binds to C4b which is attached to bacterial surface... forms CLASSICAL C3 CONVERTASE (C2aC4b). 3. This cleaves C3 into a and b. 4. C3b binds to bacterial surface, complexing with C3 convertase forming CLASSICAL C5 CONVERTASE (C2aC4bC3b). 5. This cleaves C5 into a and b. 6. C5b comibes with C6-9 to initate MAC formation. |
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C reactive protein
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activated by binding of lectins to sugar residues on microbes (e.g. phosphocholine component of LPS)
can activate Classical complement pathway: 1. CRP binds to C1 complement component activating its enz. activity (MASPs). 2. C1 can then bind and cleave C2 and C4 into a and b subunits. 3. C2a + C4b = CLASSICAL C3 CONVERTASE (C2aC4b). ** converge** 4. This cleaves C3 into a and b. 5. C3b binds to bacterial surface, complexing with C3 convertase forming CLASSICAL C5 CONVERTASE (C2aC4bC3b). 6. This cleaves C5 into a and b. 7. C5b comibes with C6-9 to initate MAC formation. |
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Type 1 IFNs (alpha and beta)
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induced by presence of dsRNA.
block spread of virus to uninfected cells: 1 activate endoribonuclease that degrades viral RNA and phosphorylating protein (eIF-2) that prevents sytnhesis of viral proteins. 2. activate NK cells to kill infected cells. |
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1 activate endoribonuclease that degrades viral RNA and phosphorylating protein (eIF-2) that prevents sytnhesis of viral proteins.
2. activate NK cells to kill infected cells. |
Type 1 IFNs (alpha and beta)
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NK cells
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large graunular lymphocytes
don't undergo T cell receptor gene rearrangement or express Ig. 2 effector functions: a) cell killing (via stim. w/ IFNalpha and beta). b) cytokine secretion, primarily IFNgamma (via stim. w/ macrophage derived IL12). |
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IFNgamma - what produces it? what does it do?
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via NK cytokine production, via IL12 stimulation of NK cells.
activates macrophages and promotes T cell response. |
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T or F: NK cells have Ab and TCRs...
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False, No Ab, No TCR.
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NK cell receptor types
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note that Nk cells require direct contact to kill.
inhibiting receptors if engaged provide signal that indicates healthy cell. activating receptors indicate cell damage etc... override inhib signals resulting in cytotoxicity. |
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Innate response timeline WRT virus infection (relative appearance of stuff)...
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1. Production of IFNalpha, beta; TNF alpha, and IL12.
2. NK cell killing of infected cells. 3. T cell killing... comes later (after innate has tapered off). |
