Micro Test Ii Arcadia

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most important component of complement

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C3

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indiv w/ deficiencies in complement susceptible to what diseases:

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1. pyogenic bacteria
2. illness involving the production of Ab's/IC's

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anaphylatoxins

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potent inducers of inflammation
-C5a, C3a
-recruit inflammatory cells, activate effector mechanisms

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C5a function/ effect

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activator of all cell types of the myeloid lineage (phagocytes)
-neutrophils respond chemotactically, degranulate, release free O2 rads
-inc. surface expression of adhesion molecules
-macs secret IL5+6
-basophils+ mast degran=histamine

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specific immunodeficiency

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abnormalities of T + B cells (cells of adaptive immune system)

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non-specific immunodeficiency

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abnormalities in complement, phagocytes,

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primary immunodeficiency

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intrinsic defects in cells of immune system; genetic

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X-linked agammaglobulinaemia

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failure of Bcell maturation
-few or no Bcells in blood/lymphoid tissues
-no IgA, IgM, IgD, IgE

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In immunodeficiency with increased IgM (HIGM)isotype, _______does not occur

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isotype switching
-Bcells cannot make the switch from IgM to IgG and IgA (mutation of CD40 ligand)

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common variable immunodeficiency (CVID)

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defects in Tcell signaling to Bcells
-Bcells not defective but fail to receive signaling
-susceptible to pyogenic infec/ intestinal protozoa

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transient hypogammaglobulinaemia of infancy

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in some infants IgG synthesis delayed up to 36 mo. (don't have mom's anymore)
-Bcells normal but lack CD4 TH stimulus
-susceptible to pyogenic infx

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Tcell deficiency

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no Tcells or poor function = opportunistic infections
-results in Bcell deficiency since require Tcell help

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severe combined immunodeficiency (SCID)

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thymus never developed
-most profound
-treatment = bone marrow transplant

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causes of SCID

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1. defect on X chromosome (50%)- defective gene encodes the gamma chain of IL2 receptor- this also forms parts of IL-4,7,11,15 receps
2. other 50% due to recessive genes on other chromosomes= deficiency of ADA adenosine deaminase or PNP purine nucleoside phosphorylase - purines degredation enzymes = accum. of dATP and dGTP= toxic to lymphoid cells

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MHC class II deficiency

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TH cell deficiency results
-develop. of CD4+TH cells depends on positive selection by MHCII molecules
-auto recessive
-children have recurrent gastrointestinal infx

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DiGeorge anomaly

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defect in thymus embryogenesis
-Tcell deficiency variable depending upon effect on thymus
-wide eyes, low ears, upper lip shortened, cardiac malform

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hereditary ataxia-telangectasia (AT)

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-breaks in chromosome 7 and 14 at site of Tcell and Ig genes (auto recess)
-variable Tcell deficiency- some IgA def., others also IgG2 and IgG4
-infants develop ataxia @18 mo + sinus, lung infx

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Wilscott-Aldrich syndrome (WAS)

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-Tcell defects and abnormal Ig levels -> small+abnormal platelets, abnormal Tcells
-eczema, pyogenic, opp infx
-X-linked

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increased susceptibility to pyogenic infections caused by deficiencies of C__ and Factor __or___

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C3, factor H or I
(C3 plays a big role in opsonization)
-all inherited as auto recess

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deficiencies in classical complement pathway results in development of ___

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immune complexes (ie lupus)
-complement normally dissolves immune complxes)

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hereditary angineurotic edema (HAE)

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C1 inhibotor deficiency
*most important deficiency of complement
-C1 inhib responsible for dissociation of activated C1
-> swelling occurs in various parts of body
-auto dominant

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chronic granulomatous disease (CGD)

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defect in ox/red pathway:
defective NADPH oxidase that catalyzes red of O2 to O2-
phagocytes incapable of forming superoxide anions (O2-)so can't kill ingested microog- they stay alive->cell med response to persistant Ag = granuloma

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Leukocyte adhesion deficiency (LAD)

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complement receptor 3 (CR3) is deficient(normally binds C3b on opsonized organisms)
-severe bacterial/gastro infx

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secondary immunodeficiencies examples

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chemo-toxic to Tcells
protein malnutrition- results in Tcell deficiency
diarrhea-lose Ig's
burns-lose Ig's
infections (AIDS)

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proteins on HIV membrane

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gp120, gp41

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cells that carry CD4

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dendritic cells, langerhans cells, microglia of CNS

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HIV cycle

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binds gp120 to CD4
enters CD+ cell, loses coat, ssDNA copy of viral RNA made by HIV reverse transcriptase, comp strand made and integrates
when Tcell activated, HIV particles made and released by budding

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effect of steroids

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dec. circ lymphocytes
dec. circ monocytes
inc. circ neutrophils
*inhibit synth of cytokines
overall= inhibition of TH cells and macrophages

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cyclophosphamide

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-alkylates DNA- interferes with strand sep during repro
-B cells more affected than Tcells, dec. lymphocytes not PMN's
*good to manage auntoAb and allograft rejection

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azathioprine

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fraudulent base in DNA- affects synthesis
-active only on dividing (cytostatic) dec. T+B cells, suppress NK + K cell activity

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methotrexate

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analog of folic acid (essential for DNA synth)
dec. in all Ig isotypes
anti-inflam cause suppress PMN's
no effect on Tcells

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cyclosporin, tacrolimus (FK506), rapamycin

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-bind to class of cytoplas proteins
-inhib Tcells and Ag presentation

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iron def.

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reduced ability of neutrophils to kill bac. + fungus, impaired NK cell activ

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selenium + copper def.

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mutations in viruses= altered virulence

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vitamin A def.

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alters epith struc= increased bac binding

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vit B6 and folate def.

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reduced cell mediated immunity

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malnutrition

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decreased #s of CD4 cells, dec in opsonization

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TH2 cells...

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secrete cytokines IL13 and IL14 --> induce Bcell prolif, favor IgE production

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Type I hypersensitivity

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mast cells bind IgE via their Fc receptors, IgE induces degranulation of mast cell, releasing mediators (typical allergic rxn)

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when allergen encounters sensitized mast cell bound w/ IgE...

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cross-links surfacebound IgE-->inc. influx Ca, triggers release of PREFORMED histamine and proteases(tryptase,chymase) and NEWLY SYNTH mediators leucotrienes and prostaglandins

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2 types of mast cells

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MMC- mucosal mast cell
CTMC- connective tissue mast cell

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the skin prick test produces...

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a wheel and flare reaction

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corticosteroids

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-suppress increase in mast cell #'s
-inhibit cytokine production incl. IL13 & IL4

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sodium cromoglycate

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prevents histamine release by inhibiting calcium influx into cell

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cyclosporin A

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inhibits expression of Il2 receptors = Bcells can't proliferate

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antihistamines

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block histamine after release

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hyposensitization therapy

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-increasing doses of allergen
-increase in allergen specific IgG and suppressor Tcell (suppress IgE response)

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Hyp Type II

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-Ab against own cells
-cytotoxic action by K cells or complement-mediated lysis
-ex. blood transfusions

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Hyp Type III

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-immune complexes deposited in tissues
-complement activated
-PMN's attracted to deposition site
-tissue damage, inflam
ex. lupus

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Hyp Type IV

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-delayed-type
-Ag-sensitized Tcells release lymphokines when encounter the Ag a 2nd time
-Tcells activating macrophages
-granulomas

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difference b/t Type II and Type III?

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II is restricted to specific cells or tissues bearing the Ag, III is against soluble Ag's in the serum

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major cause of HDN

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Rhesus system

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Goodpasture's syndrome

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nephritis from Ab's to glycoprotein on glomerular basement membrane- severe necrosis of glomerulus
(type II)

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Pemphigus

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blistering of skin and mucous membranes
-Ab's to a desmosome protein that forms junctions b/t epidermal cells
-breakdown of the epidermis

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Myasthenia gravis

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Ab's to Ach receptors on surface of muscle membranes

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immune complexes of type III due to 3 possible causes:

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1. persistent infection/weak Ab response
2. autoimmune disease (phagocytes that remove complexes become overloaded, start to deposit)
3. inhalation of Ag material (actinomyces fungi in hay, pigeon poop - IgG produced rather than IgE)

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vasoactive amines released by platelets, basophils, and mast cells cause...

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endothelial retraction = increased permeability allowing IC's to deposit on blood vessel wall

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large immune complexes removed faster or slower?

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faster because more effective at fixing complement

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IC deposition occurs where BP is ____

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high

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3 variants of Type IV:

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1. contact hypersensitivity (poison ivy)
2. tuberculin-type (72 hrs)
3. granulomatous (21-28 days)

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Leprosy

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granumolatous rxn at peripheral nerves (likes cooler areas)

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Tuberculosis

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lung- fibrosis and lesions

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Schistosomiasis

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host becomes sensitized to ova of trematode worms = granulomas

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Sarcoidosis

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tissues, lung, lymphs

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Crohn's disease

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ileum and colon

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live vaccines produce ____ and _______ immunity

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humoral, cell-mediated

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attenuation achieved by...

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mutations (large # mutations diminished virulence)

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killed vaccines produce primarily ______ immunity

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humoral

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chemicals used to inactivate pathogen

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formaldhyde = alkylating agents

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most sucessful bacterial vaccines

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inactivated toxins and toxoids

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limitation of polysaccharide vaccines

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inability to activate Th cells - activate B cells in a Tcell independent manner (not presenting Ag) = more IgM, low IgG , have to get every 4 to 5 years to boost Bcells

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recombinant antigen vaccines

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introduce gene encoding antigen of pathogen into attentuated virus or bacteria- organism serves as vector- replicates within host, expresses gene product of pathogen (also clone into yeast, ie. Hep B vx)

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DNA vaccine

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plasmid DNA encoding viral antigen injected into muscle of recipient, taken up by muscles cells and encoded protein is expressed

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anti-idiotype vaccine

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1.immunize mouse with Ag, Ab (idiotype) generated against Ag
2. immunize mouse with Ab, then anti-idiotype generated (this looks like original Ag)
3. anti-idiotype used as vaccine
-testing for HIV vaccine

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living vaccine advantage

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1. Ag challenge lasts for days or weeks
2. induces it at the right site
3. contains greatest # microbial Ag's

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killed vaccine disadvantage

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do not replicate in host
repeated boosters needed

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adjuvants

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enhance Ab production
-aluminum salts, added to Ag
1.concentrates Ag where lymphocytes exposed to it
2. induce cytokines

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commensals

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benefits from host- host does not benefit but is not harmed

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pseudomembrane colitis

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antibiotics kill normal flora of bowel
-excessive toxin released by clostridium which is normally just a minor resident --> diarrhea

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characteristics of normal flora

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1. adherence to host cells (proteins, polysacch's, pili) even thru desquamation
2.production of antimicrobial substance- inhibit other competing microbes

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characteristics of skin that inhibit microorganisms

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1. dryness
2. low pH (b/t 3 and 4 due to organic acids such as lactic acid)
3. inhibitory substances
(sweat glands secrete lysozyme, sebaceous secrete complex lipids that are degraded into inhibitory acids)

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tears contain _____ which _____

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lyzozyme, cleaves peptidoglycan

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major cause of dental caries

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streptococcus mutans
-produces glucan that acts like cement to stick bacterial cells together

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residents of adult vagina

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lactobacilli
-break down glycogen to form lactic acid

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carriers

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aquried sufficient immunity but unable to eliminate pathogen from body

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adhesins

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fimbriae, pili, cell-surface structure that bind to receptors on surface of host's cells

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antiphagocytic mechanisms

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-capsules (slippery)
-fimbriae (prevent close contact)
-siderophores- compete for iron = growth factor

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hyaluronidase

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breaks down hyaluronic acid= connective tissue glue = spread

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streptokinase

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activates plasmin, causes disolution of blood clots = spread

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coagulase

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coag of plasma = fibrin layer around cell= Ab doesn't recognize

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hemolysins

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breakdown RBC = iron

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enterotoxins 2 types:

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1. stim cAMP causing electrolyte imbalance= H2O flows in
2.inhibit protein synth = kills epith cells

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neurotoxins

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tetanus
-spastic paralysis - block inhibitory nerve impulses so fire all the time
(botulism prevents Ach release)

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pyrogenic toxins

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= superantigens --> induce secretions of TNF alpha and IL-1 = inflam, shock, death

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endotoxins

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Lipid A portion of Gram - cells
lipid A binds to macs, causing synth of TNF alpha and IL-1

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what prevents microbes from going deep into body (ie rhinovirus)

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temperature- higher temp inhibits growth inside