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152 Cards in this Set
- Front
- Back
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Structure of Ig
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4 polypeptide chains
2 heavy 2 light Arms: FAB and Fc |
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Where does Antigen bind to Ig
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Binds to FAB, antigen binding site
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IgG
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High concentration (75-80 %) in circulation at all times
a. Formed after IgM b. Neutralizes toxins by interfering with the protein binding sites, attachment, tissue damaging enzymes – very good c. Inactivates viruses – when viruses are extracelluar d. Acts as a great opsonin: bridges MO and macrophage surfaces e. The only antibody that crosses the placenta to provide newborns with passive immunity – Natural Acquired Passive Immunity – all the immunity of the mother – provides protection for several months after birth f. IgG immune response could last for years. Their presence persists over time g. A whole bunch (2,000) can activate the classical compliment pathway |
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IgM
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10% of Ig in circulation
a. First Immunoglobulin made in immune response. Use that fact diagnostically – can look for IgMs in blood for a specific disease. b. Forms a pentamer (5) of the Y shaped structures linked together at Fc ends so have 10 exposed Fab ends – large molecule c. Neutralize infectivity by interfering with the protein binding sites (attachment) i. neutralizes toxins (binding to it interferes with toxins’ functions) d. Inactivates viruses – when they are extracelluar e. When the antigen binds to the variable regions, the Fc region undergoes a conformational change and which allows it to bind to PMN’s and macrophages which assists phagocytosis. – not an opsonin f. Good activator of the classical compliment pathway – only need 1 pentamer to bind to the target to get C1q to bind. g. Presence indicates the acute inflammation phase of an illness – don’t have a lot just floating around in blood in normal times fxn= as antigen receptor |
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IgA
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very little in circulation, but important in secretions (saliva, tears, breast milk, mucus: intestinal urinary etc.)
a. In blood it forms a monomer: Y b. In circulation the monomer doesn’t last very long, ~ a few months c. Consists of 10% of IgAs d. Functions as a weak opsonin e. In secretions, it forms a dimer: >=J=< (2 Ys with the stems joined by “J” chain) f. As the dimer passes thru epithelial cells, a secretory component is added before the IgA is secreted as sIgA g. Secretory unit is there to transport it h. sIgA interferes with attachment of foreign materials to mucosal linings - neutralizes infectivity i. Does not activate the classical pathway j. So even if we have a secretory response that is very good, we will continue to have to re-develop it, if exposed after a few months. k. Breast fed infants are passively immunized as they breast feed due to sIgA – Natural Acquired Passive Immunity |
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sIgA
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In secretions, it forms a dimer: >=J=< (2 Ys with the stems joined by “J” chain)
f. As the dimer passes thru epithelial cells, a secretory component is added before the IgA is secreted as sIgA g. Secretory unit is there to transport it h. sIgA interferes with attachment of foreign materials to mucosal linings - neutralizes infectivity i. Does not activate the classical pathway j. So even if we have a secretory response that is very good, we will continue to have to re-develop it, if exposed after a few months. k. Breast fed infants are passively immunized as they breast feed due to sIgA – Natural Acquired Passive Immunity -neutralizes toxins |
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IgE
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Almost no free IgE; all of it binds to cell surfaces – cytophilic
a. IgE’s tail (Fc) binds to surface of mast cells and basophils - receptor for antigens b. Thousands of IgEs attach to the cell’s surface, presenting a wide variety of antigen binding specificities – gets acute inflammation up and running c. If an antigen binds to IgE on a Mast cell, the tail of the IgE undergoes a conformational change that stimulates the Mast cell to release its stored vasoactive substances ii. The more IgE on the surface, the more histamine can be released. Allergies are the excessive production of IgE and a proportional excessive release of vasoactive substances in response to a normally innocuous substance/antigen iii. Allergies are the result of: • To many IgE receptors on Mast cells • Host produces too many of a particular IgE • You CAN’T have an allergic reaction the first time (it could take several exposures before allergic rxn) stings before |
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IgD
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not free circulating
a. Bound to mature/immunocompetent B-cells on the surface b. Serves as a receptor (along with IgM) for antigen on B cells c. A conformational change in the tail triggers B cell activation d. One B-cell recognizes a single antigenic determinant |
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innate or natural immunity is
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1.nonspecific host resitance, 2.not acquired, 3.first line of defense
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innate or natural immunity characteristics
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1. not acquired, pre-existing, always available, 2. not specific=not directed at a particular agent
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acquired immunity results from
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results from interaction b/t cells of the imm system&components of inf or non inf Ag
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acquired immunity products
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Abs and sensitized lymphocytes
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acquired immunity characteristics
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1. highly specific, 2. requires previous exposure, 3. involves the recog'n of Ag by Ab or sensitized lymphocytes
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passive immunity is
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nonsusceptibility due lack of approp receptors
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nonspec host resistance-mechanical and chemical factors (external)
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skin, muc membr, leuk in/on muc memb, nasal hair, ciliated cells, coughing, fever, lysozyme, fa on skin, flusing of urin, saliva, terars, acidity and mobility of dg tract
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nonspec host resistance-normal microflora (external)
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presence/balance is a dynamic equilibrium, bact living on/in us are impt for competition w/pathogens for space, nutrients; normal prod'n metabolic wastes-->inhibit some pathogens
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nonspec host resistance-internal
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blood, mast cells, lymphatic system, reticuloendothelial system/mononuclear phagocyte system, other soluble factors (defensins, cathelicidins)
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nonspec host resistance-formed elements(internal)
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neutrophils/PMNs, monocytes, basophils, eosinophils, NK cells, platelets
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nonspec host resistance-plasma(internal)
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interferon, alternative complement pthwy, classical complement pthwy, acute phase proteins
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nonspec host resistance-phagocytosis (internal)
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PMNs, macrophages
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antibiotics and normal microflora
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antibiotics can kill normal flora, enabling resistant pathogens to fluorish i.e. thrush, vaginal yeast infections
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neutrophils or PMNs
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first cellular responders in acute inflamm'n, multilobular nucleus, most numerous, phagocytes
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monocytes
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phagocytic cells that migrate into tissues (not as quick as PMNs); in tissues are called macrophages, impt in transition from nonspecific defenses to acquired immunity
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basophils
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contain histamine, overresponse leads to allergic rxn w/body-wide vasodilation, decr in bp, decr bldflow to major organs, stasis, incr clotting, mobile
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eosinophils
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effective against parasitic inf, can respond in allergic rxns
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NK cells
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kill malignant cells, viral-inf'd cells, nonspecifically recog target due to abnormal cell surface (low MHC-I on surface)
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platelets
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nec for bld clotting, source of vasoactive substances and fibroblast growth factors which make collagen to promote healing
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histamine
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vasodilator, bronchioconstrictive; produced by mast cells and basophils
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interferon
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prot found in plasma that is synth'd by viral inf'd cells that inhibits viral inf in other cells, non-spec for infec agent, species specific (cannot use IF from other animals)
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complement
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complex of serum proteins that act in a seq toenhance and amplify phagocytosis, acute inflamm'n and lysis of MOs
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acute phase protein
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prot prod by hepatocytes and found in the plasma that grtly increases in [ ] in resp to early alarm mediators (i.e. complement reactive proteins CRP); APP binds MO and enhances binding of complement to MO
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complement reactive protein
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CRP facilitate the complement binding to MO and activation of the alternative pthwy
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anaphylatoxins
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soluble mediator of inflamm'n (i.e.C3a,C5a)-> induce contrx of sm m and incr vasc permeability
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why more infections in winter?
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dry->reduces mucous thickness which normally traps Mos and prevents them from contacting underlying epithelium
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purpose of the alternative complement pathway (3)
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non-specific pathway whose purpose is to generate molecules that enhace and amplify: 1. phagocytosis, 2. acute inflammation, 3. lysis of MO
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purpose of the classical complement pathway
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specific pthwy in response to reinfection - Abs bind to spec Ags
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mast cells
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non-motile, typically found in sub-cu tissue and mucosa, *critical in establishing the def supply line by releasing vasoactive substances
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lymphatic system-purpose in the imm response
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contain a lg # of macrophages and lymphocytes; where acquired imm resp begins
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reticuloendothelial system-purpose
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participant in initiation of acute inflammation
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reticuloendothelial system-players
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sm bld vessels, Kupffer cells from liver and spleen, alveolar macrophages, serosal macrophages, microglia, osteoblasts, lymph nodes (=mononuclear phagocyte system)
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phagocytosis-cell types
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PMNs, macrophages, monocytes
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phagocytosis-attachment
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same as opsonization->phago+target must make physical contact (i.e. Ig&C3b bridge)
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phagocytosis-vacuole formation
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phagosome(phagocytosed target)+lysosome(preexisting-nec for degrad'n and killing) = phagolysosome (fusion of the 2)->where killing and degrad'n takes place
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phagocytosis-nonoxidative killing and digestion
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lysozyme, defensin, Fe depriv'n, membr damage, proteolytic degrad'n
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phagocytosis-oxidative killing
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occurs in phagolysozome, much more lethal, requires inducement (i.e. C3a,C5a), phagocytes exhibit incr in ox consumption to produce an oxygen burst, highly reactive H and O intermediates needed to KILL MO but still need degrad'n Es to degrade MO
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intermediates for oxidative killing
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HClO-, O2-, H2O2, 1O2, NO
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secretion by phagocytes
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if phago has difficulty killig MO, frustration, secretes mediators of oxid and nonox killing ->tissue damage (i.e. TB tissue damage is caused by frustrated phagos)
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intracellular survival of some MOs
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i.e.TB interferes w/phagolysosome form'n, phago still senses presence TB -> secretes mediators of non-oxid killing -> tissue damage (walls off TB in a granuloma)
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death of PMNs - advantages
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NAs in exudate makes it thick so it contains foreign MOs better
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acute inflamm'n - purpose
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containment, destruction and removal of foreign material
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acute inflamm'n - order of events
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1.increased vascular permeability, 2.edema, 3.leukocytosis=chemotaxis, 4.exudate, 5.pus, 6.abcess form'n, 7.healing
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acute inflamm'n - increased vascular permeability
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release of histamine by mast cells results in vasodilation, followed by constriction of endothelial cells
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acute inflamm'n - edema
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fluid movement through spaces in capillaries out into tissues
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acute inflamm'n - leukocytosis
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PMNs bind ICAMs produces by endothelial cells, bind and then moves out of blood into the tissues (chemotaxis toward C3a, C5a)
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acute inflamm'n - exudate
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extravascular accumulation of fluid + cells to maintain viscous state and further contain defensive supply line and MOs
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acute inflamm'n - pus
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exudate+dead cells
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acute inflamm'n - abcess form'n
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large accum'n of pus which is further contained w/fibroblast and conn tissue
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chronic inflamm'n - purpose
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nonspecific containment, destruction and removal of persistent foreign material
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chronic inflamm'n - players
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T-lymphocytes, macrophages, fibroblasts
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features of acquired immunity
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1.high degree of specificity, 2.can disting b/t self and non-self, 3.involves humoral immun(Igs/Abs), 4.displays immunologic memory
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Ags - do what, best kind
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provoke Ab prod'n, lg complex prots are best, then polysaccs (lipids, NAs no good)
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vareolation
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first form of immunization in China - inf'd people w/minor form of vareola to prevent inf w/more dangerous, deadly form
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hapten
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will react w/Ab,but must bind to larger molecule first to be seen(i.e. some Abiotix)
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adjuvants
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often used w/vaccines to make the Ag bigger, more complex/foreign -> enhances immunogenicity
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B-/T-lymphocytes come from
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B from lymphoid tissue in bone marrow, T from lymphoid tissue in the thymus
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number of variable peptides in the Fab region of the heavy chain
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3 variable pp, each w/difft possible alleles; 200X4X12
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number of variable peptides in the Fab region of the light chain
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2 variable pp, each w/difft possible alleles; 200X5
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management of self-reactive Abs
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clonal deletion, anergy(arnd but inactive)
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heavy chain switch
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switch in the Fc region of the heavy chains - results in change in Ab type but not in specificity
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alternative pthwy - anaphylotoxins
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C3a and C5a
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alternative pthwy - key enzymes
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C3bBb and C3bC3bBbPr
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alternative pthwy - opsonins
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C3b enhances phagocytosis
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alternative pthwy - results
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1.enhance accute inflamm'n, 2.enhance phagocytosis, 3.cause lysis of the MO
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classical pthwy - anaphylotoxins
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C2b, C3a, C4a
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classical pthwy - key enzymes
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C1qrs, C2aC4b, C2aC4bC3b
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classical pthwy - opsonins
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none
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classical pthwy - results
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1.enhance accute inflamm'n, 2.enhance phagocytosis, 3.cause lysis of the MO
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approx# of difft Fab's
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10 million (200X5X200X4X12 = 9,600,000)
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how is autoimmunity prevented by the body?
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clonal deletion, anergy(arnd but inactive)
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TH0
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TH1
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assist macrophages in cell-mediated response
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TH2
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assist B cells in the humoral response to extracellular pathogens
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Ts
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Tctl
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primary target is virally infected cells, 2nd is malignant cells; involved in rejection of organ transplants
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Tk
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primary target is virally infected cells, 2nd is malignant cells
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Tdth
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type of TH1
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NK cells
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kill malignant cells, viral-inf'd cells, nonspecifically recog target due to abnormal cell surface (low MHC-I on surface)
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C3b stabilized by
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binding of CRP to MO, binding of C3b to polysacc on the MO
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cell-mediated immunity
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memory T cells respons
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antigen-presenting cells
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monocytes, macrophages, B cells, dendritic cell
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immunocompetent B and T cells
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B and T cells become immunocompetent when they have been exposed to and are able to recognize a specific Ag and participate in an immune response
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plasma cells
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Ab synthesizing B cells that participate in the humoral response
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IgM
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first Ig made in an immune response, best initiator of the classical pthwy (C1q binds to IgM), pentamer with 5 Fab's, monomeric IgM is found on the surface of B cells, opsonin?, inhibits infectivity by 1.binding extracellular pathogen which prevents the pathogen from binding, 2.binds a toxin preventing its action, 3.damage enzymes
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IgG
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best opsonin, most abundant Ig and is found in the blood at all times, can cross the placents, activates the classical pthwy, inhibits infectity by 1.binding toxins, 2.binding tissue damaging enzymes
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IgA
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weak opsonin, predominant Ig in external secretions, found in breast milk and secretions of allergic rxns even tho not inv'd, two forms 1.monomeric IgA in low amts in the blood, 2.dimeric sIgA in secretion (tears, saliva, breastmilk, RS and GI tracts), glandular epith'cells make the secretory component -> internalize IgA and then secrete it with the secretory component
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IgE
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all IgE is bound to the surface of mast cells and basophils (not free) which est the def supply line and do this by the release of histamine (degranulation) in response to binding of Ag to IgE on the surface
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IgD
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major membrane-bound Ig, along with IgM on mature B cells
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allergic response is a result of
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too many IgE receptors on mast cells (first exposure does not produce an allergic response -> may take several exposures)
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clonal selection
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proliferation of T and B cells specific to an Ag
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malignant cells and target for NK
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malignant cells do mot produce sufficient amounts of MHC-I which marks them for death by the NK cells
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opsonins
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C3b and Ig's (G and A, M?) enhance phagocytosis
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anaphylaxis
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body-wide anaphylaxis, Ag is usually injected (i.e. bee sting) resulting in body-wide release of histamine resulting in body-wide dilation of blood vessels causing sig drop in bp (shock) along with bronchoconstriction resulting in suffocation
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MHC
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major histocompatibility complex - primary Agenic determinant that differs from person to person
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MHC-I
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MHC-II
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cells that deal w/extracellular pthgn
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Ag-presenting cells, Th2, B-cells/plasma cells
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problems the immune system must deal with (4)
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1.extracellular pathogens(Mos on mucosal surfaces or introduced due to wound), 2.intracellular pathogens(TB or chlamydial persistance inside a phagosome w/in the mphage), 3.virus-inf'd host cells (inf'd host cells is killed as a result), 4.cancer cells (surface continuously examined by imm cells for dev'ns from norm)
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humoral immune response - cells involved
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macrophages or other APC, Th0, Th2, B-cells, plasma cells
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seq to deal w/extracellular MO: T-cell side of the humoral response
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phagocytosis of MO by Ag-presenting cell(macrophage) -> APC kills, degrades MO and presents parts on its surface in conjunction w/MHC-II -> approp Th0 recog and binds both the MH-II and foreign Ag -> binding of Th0 causes APC ro secrete IL4 -> IL4 causes Th0 to difftiate into Th2(now committed to participate in the humoral imm response altho some Th1 will still be produced) -> APC now secretes IL1 which causes Th2 to make and release IL2 receptors and IL2 (autocrine=self-stimulatory) -> binding of IL2 to IL2 receptors on Th2 causes clonal expansion of Th2 -> Th2s synth a lot of IL4,5,6,10 which act on selected B-cell clones -> drives clonal expansion of B-cells and difftiation of B-cells into Ab-secreting plasma cells and formation of memory B cells -> plasma cells secrete IgM then IgG, A and E
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seq to deal w/extracellular MO: B-cell side of the humoral response
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phagocytosis of MO by Ag-presenting cell(macrophage) -> APC kills, degrades MO and presents parts on its surface in conjunction w/MHC-II -> approp B cell binds Ag only w/IgM or IgD (not MHC-II like the Th0) -> B-cells makes receptors for IL4,5,6,10 -> IL4,5,6,10 from APC and Th2 induces B-cell clonal expansion -> after 4-5 days, B-cells difftiate into plasma cells which synth and rls IgM's -> get heavy chain switch to go from IgM (first) to IgG,A,E -> memory B-cells formed
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seq to deal w/intracellular MO: T-cell side of cell-mediated immunity
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intracellular pathogen(i.e.TB) making high amt of endogenous Ag's, therefore presented in high conc on the APC in assoc'n w/MHC-II (like phagocyt'd extracell MO) -> Th0 binds Ag+MHC-II -> APC secretes IL12 -> drives difftiation of Th0 to Th1 (still get some Th2) -> APC+Th1 causes the APC to release IL1 and make gamma-IF receptors -> IL1 causes Th1 to make IL2 receptors and rls IL2 (autocrine) -> clonal expansion of Th1s which then make gamma-IF which attacts and activate mphages -> gamma-IF cont to stim and attact mphages pushing them to RS burst and making them cap of ox killing (better killers), TB is an example
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seq to deal w/intracellular MO: B-cell side of cell-mediated immunity
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B-cells are not needed/involved
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seq to deal w/viral infection
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viral and host proteins are synt'd and presented in conjuct'n with MHC-I -> Tctl=Tk binds Ag+MHC-1 -> Tctl makes IL2 receptors and releases IL2 (autocrine response) and makes more perforins and granzymes -> clonal expansion of Tctl -> Tctl releases perforins (like MAC) and granzymes (contain hydrolytic enzymes in cytoplasmic granules) onto the surface of the target -> lysis of the target = example of cell-mediated immunity (no B-cell involvement), Tctl's also respond to gamma-IF and IL2 from Th1 which are created as a result of ingested cellular debris created by killing by Tctl action
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presentation of processed vs synthesised Ag's
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processed Ag's are presented in conjunction w/MHC-II (difft'n to Th1 vsTh2 depends on the density of presentation), synthesized Ag's are presented in conjunction w/MHC-1
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virally inf'd cells are taken care of by
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NK cells and Tctl cells - activity of both is enhanced by gamma IF and IL2
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seq to deal w/cancer cells
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malignant cells do not produce sufficient amounts of MHC-I -> attract attention of NK cells which survey cells -> release of perforins and granzymes (Tctl cells can also kill malignant cells, but are not the major line of defense) -> NK cells also respond to IL2 and can culture NK cells with human tumor tissue w/high [IL2] to make them more targeted to the tissue when injected into the pt
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Tctl vs NK cells
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Tctl cells are the primary defense against viral infections, and NK cells are the primary defense against malignant cells
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naturally acquired active immunity
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immune response
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naturally acquired passive immunity
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IgG crossing the placenta, sIgA in mother's milk
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artificially acquired active immunity
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immunizations
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artificially acquired passive immunity
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Ig's from someone else
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killed vaccine
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pathogen is killed by heat or highly purified Ag -> vaccine contains nothing infectious, only Ag -> host response yields Ab only (i.e.Salk)
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attenuated vaccine
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use a mutant inf agent that cannot cause disease, but will still infect -> yields both Ab and cell-mediated immunity (i.e.Sabin)
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hybrid vaccine
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can take vaccinia virus and add genes for other organisms that code for immunogenic proteins -> yields both Ab and cell-mediated immunity
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primary immunodeficiency
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congenital
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secondary immunodeficiency - natural causes
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are acquired (HIV, malignancy of B,T and plasma cells, severe malnutrition, uncontrolled diabetes, pregnancy, stress, aging)
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secondary immunodeficiency - other causes
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immunosuppressants, chemotherapy, splenectomy, irradiation, severe burns, steroids
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primary B cell immunodeficiency
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Infantile X-linked agammaglobulinemia
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primary T cell immunodeficiency
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DiGeorge Syndrome (congenital thymic aplasia)
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primary B and Tcell immunodeficiency
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SCID = severe combined immunodeficiency
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hypersensitivity
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excessive or inappropriate reactivity resulting in tissue damage - i.e. allergies
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type I hypersensitivity
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mediated by IgE, mast cells and basophils
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type II hypersensitivity
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mediated by IgM, IgG, complement, PMN & Mθ
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type III hypersensitivity
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mediated by IgM, IgG, complement, PMN & Mθ
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type IV hypersensitivity
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Th1 (Tdth) lymphocytes & Mθ (i.e. TB)
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for which Ig classes do phagocytes have receptors?
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IgA, IgG and IgM
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Ig class most directly assoc's w/dil'n of capillaries
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IgE
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which Ig's are found on the surface of mature, immunocomp B cells
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IgD and IgM
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Ig's likely to be responsible for neutralizing infectivity of extracellular virus
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IgM, IgG and IgA
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Ig most responsible for est the def supply line
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IgE
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site of Ig synthesis
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most Ig synthesis takes place in the lymph nodes, away from the site of infection
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Ig's most likely to activate the alternative complement pthwy
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none
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fetus acquires which Ig
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IgG
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breast milk contains which Ig
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sIgA
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Ig class first formed in an imm resp
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IgM
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Ig class that greatly increases w/subsequent exposure
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IgG
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anamnestic imm response occurs when w/immunizations
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injections after the first
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types of Ag's in immunization
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large, complex prots and polysaccharides
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on switch cell of the imm response
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Th
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ac inflamm: edema serves to deliver
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Ig's, components of the complement system, fibrinogen, plasminogen
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antigenic stimulation in the gut results in sec'n of sIgA where?
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gut, upper Rs tract, saliva, genito-urinary tract
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what do platelets do?
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release vasoactive substances, clot formation, promote healing, release fibroblast growth factors
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