Immunology Flashcards
Innate immunity relies on what 2 cell types? Response time? What 3 things produced by virally infected cells protect uninfected cells and activate macrophages and NK cells?
Phagocytes and natural killer cells (NK), non-specific instinctive rapid response, resistance not improved by repeat infection
Lysosomes, complement, interferon
Response time of adaptive immunity? Neutrophils take up what % of the blood? Lifespan? Important role in what? Has what 2 main intracellular granules? Contain what? Primary lysosomes combine with what? Have what 2 receptors? Kill microbes by secreting what?
Days-weeks, resistance improved by repeat infection
65%, 6 hours- 12 days
Innate immunity- phagocytosis
Primary lysosomes- myeloperoxidase, muramidase, acid hydrolysis and proteins (defensives), with phagosomes containing microbes to digest them
Secondary granules- lactoferrin and lysozyme
Fc and complement receptors
Can kill microbes by secreting toxic substances (superoxides)
Monocytes take up what % of blood? Lifespan? Play important role in what? Differentiate into what in the tissues? Main role is to what? Have what that can kill microbes? Have what receptors to bind to all kinds of microbes?
5%
Months
Innate and adaptive immunity
Macrophages
Remove anything foreign or dead
Lysosomes containing peroxidase that can kill microbes
Fc, complement, PRRs, Toll-like receptors, mannose receptors
Lifespan of macrophages? Examples? Important role in what? Most often do what? Main role? Have lysosomes containing what? Have what receptors? Present what to T-cells?
Months/ years
Kupffer cells (liver) and microglia (brain)
Innate and adaptive immunity
First line of non-self recognition
Remove foreign (microbes) and self (dead/ tumour cells)
Have lysosomes containing peroxidase (free radicals)
Fc, complement receptors, Toll-like receptors and mannose receptors- can bind to all kinds of microbes
Antigens
Eosinophil make up what % of blood? Lifespan? Granules stain for what dye type? Mainly associated with what infections?Granules contain what protein potent to what organism? What does MBP activate, induce and provoke?
5%
8-12 days
Acidic dyes e.g. eosin- red/ pink
Parasitic and allergic reactions
Major Basic Protein (MBP)- potent toxin for helminth worms
MBP activates neutrophils and induces histamine release from mast cells and provokes bronchospasm (allergy)
Basophils make up what % of blood? Lifespan? Granules stain for what dye type? Similar to what? Express what receptors? Binding of IgE results in what? Mainly involved in immunity to what? Difference compared to mast cells?
2%
2 days
Basic dyes e.g. haemotoxylin- blue/ violet
Mast cells
High affinity IgE receptors
De-granulation- release of histamine–> allergic reactions
Parasitic and allergic reactions
Mast cells= fixed in tissue, whereas basophils are able to circulate in blood around the body
Mast cell express what receptor? Only where? Binding of IgE receptor results in what? Mainly involved in what immunity?
High affinity IgE receptors
Tisses
De-granulation–> histamine release, main cause of allergic reactions
To parasitic and allergic reactions
T lymphocytes make up what % of blood? Lifespan? Major role in what? Originate and mature where? Recognise what cell type? Bind antigen through what? Produce what? Specifically kill what? 4 T lymphocyte types?
10% Hours- years Adaptive immunity Bone marrow and thymus APCs T cell receptors (TCRs) Cytokines Infected host cells Th1, Th2, cytotoxic and T reg cells
TH1 and TH2 cells do what and have what receptor? Cytotoxic T cells use what receptor to kill cells directly? T reg cells do what and are found where?
Help B cells make antibody, activate macrophages and NK cells, help develop cytotoxic T cells
CD4= help immune response for intracellular pathogens
CD8
Regulates immune response and acts to dampen them- blood, lymph nodes and spleen
B lymphocytes make up what % of the blood? Lifespan? Major role in what? Originate and mature where? Recognise what? Express what on cell surface? Differentiates into what to make antibodies? Found where?
15% Hours- years Adaptive immunity Bone marrow APCs Membrane bound antibody on cell surface Plasma cells that then make antibodies Blood, lymph nodes and spleen
NK cells account for what % of lymphocytes? Expresses what glycoprotein? Found where? Recognise and kill what 2 cells via apoptosis?
15%
CD56
Spleen and tissues
Virus infected and tumour cells
Dendritic cells are type of what? Only these cells can do what? They produce cytokines and other factors that promote what? Found in tissue that has contact with what?
APC
Induce primary immune response inactive or resting T lymphocytes
B cell activation and differentiation
Outside environment e.g. over skin (in Langerhans cells) and in linings of nose, lungs, stomach and intestines
What is complement? Derived from what and more than how many types? Many exist as what? Once activated may behave as what? Each precursor is cleaved into what? Major fragment ‘b’ has how many biologically active sites? Minor fragments ‘a’ have important biological properties in what phase?
Complex series of interacting plasma proteins which forms major effector system for antibody- mediated immune reactions
Liver, more than 30
Inactive precursors- enzyme which cleaves several molecules of next component in sequence
Into 2 or more fragments
2- one for binding to cell membranes/ triggering complex and the other for enzymatic cleavage of next complement component
Fluid phase
Control of complement activation involves what? Major purpose of complement pathway? 4 things that complement can do when coming into contact with pathogen?
Spontaneous decay of any exposed attachment sites and inactivation by specific inhibitors
To remove/ destroy antigen, either by direct lysis or by opsonisation
Lyse microbes directly (Membrane Attack Complex- group of proteins make hole causing inrush of fluids–> lysis)
Increase chemotaxis (C3a and C5a)
Enhance inflammation
Induce opsonisation (C3b)- antigen becomes coated with substances, more easily engulfed by phagocytic cells since macrophages
Clinical indications related to complement?
Recurrent infections in children (especially pulmonary)
Swelling in hands or face
Fatigue, butterfly-shaped rash on face, cold sensitivity in extremities
Fever, tachycardia after blood transfusion
Recurrent infections in end-stage liver disease (cirrhosis, hepatitis)
Morning urine colour
Complement activation occurs in what 2 sequential phases? The C3 is cleaved by what enzymes? Major fragment C3b mediates what vital biological activities? Minor fragment C3a acts to do what? Cleavage of C3 is achieved via what 3 main routes?
Activation of C3 component
Activation of the ‘attack’ or lytic pathway
C3 convertases
Opsonisation and lysis of pathogen–> membrane attack complex
Enhances inflammation
Classical, alternative and lectin pathways–> C3 convertases, in response to different stimuli
Activation is dependent on what? Activation can be antibody independent when what 3 things react directly with C1? Complement proteins involved? Antibody more efficient at activating C1q than IgG? Antibodies that don’t activate the classical pathway? What is the classical pathway C3 convertase?
Antibodies Polyanions (e.g. heparin, protamine, DNA and RNA from apoptotic cells,) gram-negative bacteria or bound C-reactive protein C1, C2 and C4 IgM IgA, IgD and IgE C4bC2a= cleaves C3--> C3a and C3b
Alternative pathway consists of what 4 things? What is the central reaction in this pathway? It generates a C3 converts without the need for what? What are the most important activators? Alternative pathway= responsible for what? Active enzyme involved?
Factor D, factor B, properdin (factor p) and C3
Antibody, C1, C4 or C2
Microbial cell surfaces e.g. yeast walls, bacterial cell walls or endotoxin (found in gram-negative bacteria)
Innate defence
C3bBb- stabilised by properdin
Activation in lectin pathway is independent of what? Consists of what 5 things? Initiated when what binds to mannose on bacterial cell walls, yeast walls or viruses? C3 convertase involved?
Mannose-binding lectin (MBL), MASP-1, MASP-2, C4 and C2
Mannose-binding lectin (MBL)
C3a along with C5a acts to enhance what? By stimulating what? This increases what? C3b has what which is used to bind to the pathogen surface? Used in what process to coat the pathogen surface?
Inflammation
Mast cells to secrete histamine–> increased vascular permeability and attracts leucocytes
Thioester bond
Opsonisation
2 receptors on macrophages for complement proteins? Macrophage cannot engulf protein coated in what on its own? How can phagocytosis be performed?
CR1 and a C5a receptor
C3b
C5a–> C5a receptor, so C3b can bind via CR1 receptor to enable phagocytosis
C3b can also bind to what complex? Forms what is known as what? Can do either what or what? What forms the MAC?
C4bC2a complex–> C4bC2aC3b complex
C3/C5 convertase
Cleave C3–> C3a and C3b or C5 into C5a and C5b–> MAC formation
C5b together with other complement proteins–> lysis and pathogen destruction
Recurrent infections caused by what bacteria? 3 e.g.? Due to what? Common in young children why?
Encapsulated bacteria- mainly gram negative
Meningococci (Neisseria meningitis), haemophilus influenza b, strep. pneumonia
Due to gap between loss of maternal antibodies and antibody production
C5-C9 deficiency leads to what 2 infections? Deficiency of what leads to neisseria infection? C3 deficiency leads to what? C2 deficiency? Factor I deficiency? % of recurrent meningococcal infections have complement deficiency?
Neisseria and haemophilus influenza B infections
Factor B, D and properdin
Recurrent bacterial infections, wider immune problems
Strep infection (especially pneumoniae)
Upper UTIs and glomerulonephritis
30%
Symptoms and median survival or paroxysmal nocturnal haemoglobinuria?
Fatigue, erectile dysfunction and abdominal pain- 10 years
Young adult onset
Excessive clotting- no control of complement activation, RBCs lysed–> clots
What causes atypical haemolytic uraemia syndrome (aHUS)? Leads to what? Inheritance?
Factor H, factor I, factor B, C3 autoantibodies or mutation
Abnormal clot formation in small blood vessels–> acute kidney failure–> end-stage kidney disease
Autosomal
What causes dense deposit disease (DDD)? Onset age? % develop end-stage renal disease? Causes what?
C3 and factor H polymorphisms, lipodystrophy (complete/ partial loss of adipose tissue)
5-15 years
50%
Uncontrolled activation of complement in certain tissues
What causes hereditary angiodema? Deficiency of what? C1 inhibitor deficiency leads to what? Inheritance? Depletion of what are diagnostic? Also inhibits what? What production?
Deficiency of complement control proteins
Excessive complement activation via classical pathway
Autosomal dominant
C2 and C4
Coagulation cascade
Bradykinin
What is systemic lupus erythematous (SLE)? Complement deficiencies in what cause predisposition for SLE? Results in what?
Autoimmune disease
C1q, C2 and C4
Impaired clearance of apoptotic cells and immune complexes
More prevalent in females
