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76 Cards in this Set
- Front
- Back
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What are the primary lymphoid organs?
What happens there? |
Thymus and bone marrow.
All leukocytes are produced and mature here (T cells in thymus). |
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What are the secondary lymphoid organs?
What happens there? |
Lymph nodes, spleen, Peyer's Patches in tonsils, appendix, and small intestine.
Lymphocytes intercept pathogens here. Strategetically placed at potential sites of invasion. Houses macrophages and other immune cells. |
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Describe the circulation of lymph.
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Excess interstitial fluid leaves capillaries and enter the tissue,
And are drained into lymphatic capillaries, becoming "lymph". Lymph are then drained by lymph capillaries into larger lymph vessels, Filtered through lymph nodes to remove antigens, And eventually returned to the circulatory system. |
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What happens in lymphoedema?
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Lymphatic vessels don't function properly,
Antigens not delivered to lymph nodes, which don't learn about infection So lymphocytes aren't activated Affected tissue risk uncontrolled infection. |
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Apart from lymph, what stuff also enter the lymphatics and go to lymph nodes, via the one-way valves of the lymph capillaries?
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Plasma proteins, pathogens, dendritic cells (antigen-presenting).
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What clears antigens in the lymph nodes?
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Phagocytes (neutrophils and macrophages).
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L capillaries -> (one-way valves) -> L vessels
L nodes are scattered throughout larger L vessels Where do the lymph eventually drain to? |
Circulatory system via large neck veins.
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What does the Thymus do?
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Lymphocytes (T cells) mature and multiply here
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What 5 things do the Spleen do?
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Immunological/Antigen presentation
Makes immune components (including antibodies and lymphocytes) Filtration of blood (RBC filtering and removal) (healthy RBCs can deform and squeeze through splenic vessels) Cleaning blood of old RBCs, debris, and infectious agents (by large phagocytic reticular endothelial cells) Blood pooling (reservior) |
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Describe the development of the Thymus.
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Most active (max size) during puberty.
Atrophies with age - becomes fibro-fatty tissue |
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What 2 things do Lymph Nodes do?
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Immunological/Antigen presentation (Provides site for T and B cell activation by antigens)
Filtration of lymph (cf. Spleen filters blood) |
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What are the 3 causes of Lymph Node enlargement?
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Follicular Hyperplasia (B cell response, cos they are majority there)
Paracortical Hyperplasia (T cell response) Sinus Hyperplasia Hyperplasia: Abnormal increase in number of cells |
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What do special L capillaries (of small intestines) called Lacteals do?
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Transports absorbed fats to the blood.
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Why are there more afferent lymphatic vessels than efferent?
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Lymph gets to travel in faster but leave slower,
allowing for extra time of antigens by macrophages, lymphocytes, and dendritic cells. |
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L nodes: What happens at the deep cortex?
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Lymphocytes exit blood circulation and enter the L node here.
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L nodes: What are germinal centres?
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Mass of B cell proliferation in the lymphoid follicle (between subcapsular sinus and deep cortex), when antigens are encountered.
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How do red pulp's splenic cords (reticular fibres laced with macrophages) filter red blood cells?
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RBCs must deform to fit through these cords, in order to get to the venous sinusoids, and return with the blood to circulationm
M-phages recognise aged RBCs and platelets. Aged RBCs break into fragments when squeezing into sinusoids, and the debris is eaten by m-phages |
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Spleen: Why does white pulp look darker than red pulp?
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Cos of dark-staining nuclei of densely-packed lymphocytes.
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List 3 factors that makes skin resist pathogens
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Tough-bastard keratin, outer-most protein layer that is abrasion and water-resistant
Tight intercellular junctions Skin secretions: Acidic, chemicals making skin inhospitable to pathogens - One secretion is lysozyme, enzyme that digests cell wall of some bacteria. |
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What is the enzyme lysozyme found in?
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Virually all body secretions: Sweat, mucus, saliva, milk, etc.
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Mucous membranes line digestive, respiratory, urinary, and reproductive tracts. Name an immune property of MM.
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MM secretions are acidic and contain lysozyme (eats some bacterial cell walls)
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Name special immune properties of some surface membranes
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In stomach, low pH and digestive enzymes.
Digestive and respiratory passageways, sticky mucus that traps pathogens - for swallowing and digesting |
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Name general properties of the innate immunity.
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Fast-acting
Non-specific Crude defense against anything and everything |
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Name the 5 types of innate defense.
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1. Phagocytic cells (esp. neutrophils and macrophages)
2. NK cells - kills traitors (virus-infected or cancerous cells, and transplanted organs) Non-cellular: 3. Antimicrobial proteins and compliment Non-cellular & Non-protein: 4. Fever 5. Inflammation |
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Describe neutrophils
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Most abundant immune cells (50-70% of WBCs)
Normally not found in healthy tissues First to leave blood and enter tissue at site of infection or trauma Recruited by chemicals released by m-phages and injured tissues Short-lived: Can only phagocytose a few cells before dying |
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Describe monocytes/macrophages
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The monocytes follow neutrophils into affected tissue
Turns into macrophages Reinforces resident macrophages Unlike neutrophils, m-phages usually present in tissues Can be free Ms and wonder in blood Or fixed, like Kupffer cells in liver, or microglia in brain |
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Describe attack properties of neutrophils and macrophages
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Phagocytose pathogens and kill with lysosomal enzymes and highly reactive chemicals
If pathogen too large (e.g. parasite), can also excrete enzymes externally |
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What do phagocytes use to differentiate pathogens and normal cells
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Special cell membrane receptors: Mannose receptors, and Toll-like receptors.
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Name 2 processes that occur when phagocytes recognise a pathogen.
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Ingestion of pathogen
Release of chem alarm signals that mobilise other cells of innate and adaptive immunity |
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What's a phagosome?
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A phagocytic cell's vesicle that traps pathogens
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After engulfing the pathgens, what killing techniques do the phagocytes emply?
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1. Pumping H+ into the phagosome (kills some bacteria directly, makes replication difficult for survivors)
2. Enzymes convert O2 to toxic reactive oxygen intermediates (e.g. superoxide anions, hydrogen peroxides, hydroxyl radicals) - process called Respiratory Burst. Other enzymes produce toxic nitric oxide (which diffuse into phagosome) 3. Phagosome fuses with lysosomes to form phagolysosome, where: - hydrolytic enzymes digest pathogen - Defensins poke holes in bacterial membranes - Enzymes convert reactive oxygen intermediates to chemicals similar to bleach (fuck yes) |
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What does opsonisation do, and why is it useful?
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A process whereby molecules from immune system coat bacteria to provide hand-holds to improve phagocytosis.
Cos some bacteria evolve capsules, making them slippy hard-to-grab bastards. |
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What are 2 types of opsinins*?
*Coats bacterial capsule to enhance phagocytosis |
Antibodies and compliment
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Name some strategies that pathogens have evolved to escape phagocytosis.
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Secreting molecules that block phagosome-lysosome fusion
Developing resistance to effects of lysosomal enzymes and reactive oxygen intermediates Finding ways to escape the phagosome, Take up residence Replicate within phagocyte cytoplasm (TB bacteria can replicate inside macrophages) |
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How does body deal with anti-phagocytosis strategies?
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Certain T cells of adaptive defense mechanism can enhance entire killing mechanism of macrophages.
This enhancement only happens when the m-phage presents that bacteria to the T cell (another e.g. of innate-adaptive immune system interactions) |
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Why are NK cells unusual?
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Are a type of lymphocyte (group of WBCs, including T and B cells, mediates adaptive immunity), yet involved in innate immunity.
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NK cells are lymphocytes like B and T cells. How are NK cells different?
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NK cells are larger,
Its cytoplasm contains granules It doesn't express antigen receptors (both T & B do), but can still recognise abnormal cells |
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How are B and T cells different?
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B cells attack extracellular pathogens.
T cells attack cells (infected or cancerous). |
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How do NK cells identify traitor cells (infected or cancerous)?
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Via the absence of self-proteins (suppressed when cells become rogue or hijacked).
NK cells kill the cell if it doesn't express self-proteins on surface. |
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Immune surveillence: NK and T cells both scan cells for abnormalities.
What's the difference in process between the 2 cell types? |
T cells look for presence of abnormal antigens on cell surface.
NK cells look for absence of normally-occuring self-proteins. |
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Name the 7 stages of viral replication:
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1. Attachment/adsorption
(depends on cell tropism - involuntary response) 2. Penetration 3. Uncoating 4. Transcription and/or translation (depends on viral genome type) 5. Genome replication (again, depends on viral genome type) 6. Assembly 7. Release (lysis of host cell, or budding [host membrane + embedded viral proteins]) |
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NK and cytotoxic T cells both kill via same mechanism, which is?
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Direct contact and forces apoptosis.
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Why are NK cells important?
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Key in early response to pathogens.
Continues to play role after T and B cells are activated. |
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Like m-phages, NK cells become more effective killers following what process?
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Activation by cytokines from certain T cells.
Coating infected cell with antibody. (2 e.g. of innate-adaptive immune response interaction) |
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Antimicrobial proteins: What are interferons?
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Cytokines that:
Messes with viral replication Modulate inflammation Active immune cells |
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Name the 3 types of interferons?
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Alpha, beta, and gamma.
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What do gamma interferons do?
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Acts in various ways to signal other immune and non-immne cells.
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Name and explain the 9 bacterial virulence factors
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Appendages
(pili for adhesion in gram -ve) (flagella = motility) Invasins (invade host cell) Capsule (antiphagocytic) (also masks compliment and antibody) Toxins (exotoxin = both G +ve & -ve) (endotoxin = only -ve) Immunostimulatory surface proteins (teichoic acids in +ves) Nutrient competition Phase variation & antigenic variation (immune defence evasion) Endospore formation (very hard to kill) Transfer of antibiotic-resistant genes (transformation, transduction, conjugation, transposition) |
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What are the fates of T cells who pass or fail positive and negative selection?
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Fail: Apoptosis
Pass both: Allowed to mature. |
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What 2 things must mature B and T lymphocytes accomplish to be successful?
Either success or apoptosis |
1. Generate a viable antigen receptor by randomly shuffling its DNA
2. Survive the education process (tests immunocompetence [can recognise antigens by binding] and self-tolerance) |
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T cell education:
What does positive selection entail? |
Only T cells that recognise self-MHCs (and bind to it) can survive
Tests whether cell can recognise antigens (presented by MHC proteins) Test adminisered by antigen-presenting cells (e.g. dendritic cells) |
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T cell education:
What does negative selection entail? |
Only T cells that don't react to self-antigens (and bind to it) can survive
Tests whether cell is self-tolerant Test also adminisered by antigen-presenting cells (e.g. dendritic cells) |
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What are complements?
What do they do? |
A group of serum proteins.
Activated by range of foreign molecules Functions: Activates inflammation Destroys cells (via lysis) Participates in opsonisation (tagging target cells with receptors) |
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How do complements work?
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C proteins respond in sequential manner = produce reaction casade
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Complement proteins contain C1 to C9 - how were they named?
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Order of discovery - not function.
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Explain complement Classical Pathway.
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C1 activates when bind to antigen-antibody complex)
Active C1 cleaves C2 (C2a & b) and C4 (C4a & b) C2b + C4b = protease "C3 convertase" C3 convertase cleaves C3 (C3a & b) |
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Explain complement Alternate Pathway.
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C3 -> C3a and C3b
(Constant process, but a and b are soon destroyed w/o activation) Antigens (endotoxins, polysaccharides, cell wall components) react with C3b. C3b then reacts with - Factor B - Factor D - properdin forming complex called "C3 convertase" C3 convertase cleaves C3 (C3a & b) |
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Explain sequences in both complement pathways (Classical and Alternative), after the cleavage of C3.
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C3a involved in stimulating inflammation.
C3b - Reacts with other complement components to form C3 convertase - Attaches to microbe surface (Phagocytes have binding site for C3b) = C3b facilitates opsonisation, by binding microbes, then getting phagocytosed C5 convertase = C3 convertase + properdin - Cleaves C5 into a and b C5a - Enhances inflammation - Act as chemoattractant for phagocytes C5b - Reacts with other complement components (inc. C6 to C9) to form Membrane Attack Complex (punches holes and causes cell lysis) |
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Summarise complement functions, after generation of C3 convertase
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Recruitment of inflammatory cells
(C3a, C5a) Opsonisation for phagocytosis (C3b, C5a) Cell lysis via Membrane Attack Complex (C5b + C6~9) |
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What triggers the production of interferons?
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Virus enters cell, and produces structures not found in uninfected cells. These viral material stimulates interferon production.
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What do interferons do?
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Disrupts viral replication.
Mechanism: Moves out of cell Attaches to receptors of similar cells nearby Original infected cell can't save self Cells with interferon bound to surface protects against viral invasion: - Production of enzymes degrading messenger RNA - Enzymes preventing protein synthesis So, virus can still enter cell, but completion of viral replication prevented |
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What are phagocytes attracted to?
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Chemical products of microbes.
Phospholipids released by injured mammalian cells Components of compliment system |
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What surface receptors mediate phagocyte attachment?
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Antibody
Lipopolysaccharides Complement receptors (e.g. C3b) |
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Adaptive Immunity:
Explain Cytotoxic T-cell mechanism |
Virus infects cell and synthesises viral proteins - some proteins degraded to peptide fragments
These peptide fragments are complexed with target cell's MHC class 1, and displayed on cell surface. Cytotoxic T cells interact with target cell by recognising both: - class 1 MHC - viral antigen The Cytotoxic T cell then release - cytotoxins (induces apoptosis) - perforin (causes cell membrane proforations) |
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Contrast MHC classes 1 and 2
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MHC class 1:
- On all nucleated cells - Typically presents peptides from intracellular sources (e.g. viral matter inside own cell) MHC class 2: - Present on all professional APCs (dendritic, m-phages, B cells) - Typically presents peptides from extracellular sources - engulfed stuff (e.g. bacteria) |
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What are cytokines?
What are the 2 types? |
Proteins made by cells; that affect cell behaviour
1. Interleukins: Cytokines between leukocytes 2. Chemokines: Chemotaxic factors |
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What do acute-phase proteins do?
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Activates complement system.
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What do activated T Helper-1 cells do?
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[Executive Generals]
Secrete IL-gamma: Activates macrophages to Kill Mode Also secretes IL-2: - Promotes TH1 and cytotoxic T cell response - Inhibits TH2 cell response Other secretions: - IL-3: M-phage proliferation in bone marrow - MCF (M-phage Chemotactic Factor): Chemotaxis, m-pahge accumulation at site of infection - Tumour Necrosis Factor alpha: -- Local inflammation, -- Endothelial activation, -- Nitric Oxide production in m-phages [Weaponise] |
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What do activated T Helper-2 cells do?
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[B cell messengers]
Secretes IL-4 and IL-5: - Stimulates B cell activation - Inhibits TH1 cell response |
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What does B cell activation lead to?
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Clonal expansion, and differentiation into
- Antibody-secreting plasma cells [Factories] - Long-lived memory cells [Sages] |
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Antibody isotypes:
Describe IgM |
Pentamer or membrane-bound
Primary immune response Low affinity, high avidity (binds quickly but weakly) |
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Antibody isotypes:
Describe IgA |
Dimer (A dime)
Found in intestinal tract and ALL SECRETIONS Acts through neutralisation |
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Antibody isotypes:
Describe IgD |
Membrane-bound
Similar structure to IgG |
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Antibody isotypes:
Describe IgG |
Most common species
Secondary immune response (takes over after IgM) Able to cross placenta |
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Antibody isotypes:
Describe IgE |
Triggers histamine release from mast cells
Involved in allergy and anaphylaxis |
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Can B cells only make one isotype of antibody?
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No, they can switch production types: (class-switching/switch-recombination)
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