Term
| Define the difference between antigenic shift and antigenic drift. |
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Definition
antigenic shift: occurs when RNA segments are exchanged b/t viral strains in a secondary host --> no cross-protective immunity to virus expressing a novel hemagglutinin --> serious pandemics
-e.g. swine flu, avian flu
drift: mutations alter epitopes in hemagglutinin so that neutralizing Ab no longer binds --> partial immunity, typical flu. Pt must undergo new primary immune response to clear mutated virus (1-2 wks) |
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Term
Know the difference between a primary infection and latency.
why are neurons a good place for viruses to hide?
EBV (what does this produce in adults, latency) |
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Definition
Latency: pathogens cease to replicate until immunity wanes
-e.g. herpes simplex, initially infect epithelia, spreads to regional sensory neurons
-recurrence of infection
-chickenpox, shingles, herpes
-not a true immunodeficiency, virus is "hiding"
Neurons lack MHC I, can't be killed by CD8T cells
In adults, produces infectious mono, an acute infxn of B lymphocytes by EBV binding to CR2 of BCR -> B cells proliferate -> T cells specific for EBV proliferate -> mononucleosis (mainly T cells)
-a few B cells become lately infected, shut down everything except EBNA-1
-the proteosome can't degrade EBNA-1 into peptides that can be presented by MHC I molecules/killed by CD8 |
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Term
| GVHD (graft vs host disease) |
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Definition
caused by *mature T cells in a BM* donor transplant that respond to the allogeneic MHC class I & II molecules of recipient
Caused by mismatch of MHC I, MHC II and minor histocompatability antigens |
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Term
| Know how some organisms can subvert the immune system |
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Definition
M. tuberculosis prevents phagosome-lysosome fusion
Listeria escapes from phagosome into cytosol, grows & replicates, is eventually killed by CD8
CMV has a variety of ways of preventing MHC I from presenting Ag to CD8 T cells
-prevents MHC I synthesis or causes its degradation
-a second group of proteins prevents NK cells from mounting a back-up response
suppress immunity: (staphylococcal toxic shock is a "superantigen," HIV leads to gradual loss of immune competence, leading to opportunistic infxns)
induce immunopathologic responses (inflammation initiated against RSV, schistosome can damage tissues, organs) |
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Term
| Define bacterial superantigens |
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Definition
bind nonspecifically to TCR, causing CD4 T cells to produce suppressive cytokines (IL-1, IL-2, TNF-alpha)
overwhelms immune system, can lead to *systemic/septic shock*
Suppresses a useful adaptive immune response (T cells bound to super Ag die w/o specific stimulation, removing many Ag specific T cell clones)
-body tries to shut it down, leads to state of immunosuppression |
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Term
| Know the difference between primary inherited immune deficiencies and secondary immune deficiencies |
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Definition
primary: due to defective inherited genes
secondary: environmental factors (e.g. immunosuppressive drugs) |
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Term
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Definition
lack C3, an opsonin that promotes the phagocytosis of bacteria by macrophages & neutrophils
recurrent infxn with Gram-neg bacteria
susceptibility to capsulated bacteria |
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Term
| Type IV hypersensitivity reaction |
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Definition
Caused by effector T cells
-mostly CD4 Th1
-minority are CD8 mediated
peaks 48-72 hrs ("DTH")
pro-inflammatory cytokine production (IFN-g) and macrophage activation by Ag specific Th1 cells
recruitment, activation of non-specific inflammatory leukocytes (PPD skin rxn, contact dermatitis, poison ivy/oak, gluten sensitivity)
-tuberculin test: Th1 recognize peptides from M. tuberculosis presented by HLA II |
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Term
Describe acquired immune deficiency syndrome (AIDS) and the HIV infection process
-sx in primary infxn?
-how does HIV infect cells? (and which cells does it infect?)
-resistance? |
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Definition
Primary infxn is primarily asymptomatic with mild flu-like sx (acute retroviral syndrome)
HIV uses CD4, CC-CKR55 to infect CD4 T cells, dendritic cells, and macrophages (brain cell, intestinal epi, lymphatic tissue also targets)
-"macrophage-tropic"
genetic def in CCR5 (the co-receptor for macrophage-tropic HIV variants) confers resistance
HIV = lentivirus (slow disease) member of Retrovirus family
-latent by forming a provirus within target cell
-when activated, T cells induce the transcription of the provirus, leading to replication
results from the gradual loss of CD4
results in opportunistic infxns, ultimately leading to death if untreated |
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Term
| Type II hypersensitivity reactions |
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Definition
IgG or IgM mediated; caused by Ab directed against components of cell surfaces or ECM
small reactive molecules (e.g. penicillin, other drugs) bind to cell-surface components of human cells, are recognized as foreign, B-cell response produces IgG
Ab binds to host cell (usually RBC) and cells that recognize Fc promote killing of the cells
C3b, Th2 cells stimulate Ag-specific B cells, classical pathway
diseases: drug allergies, hemolytic anemia, blood transfusion rxns, hemolytic disease of newborn
Autoimmune: Ab sticking to and blocking receptor
Hemolytic: autoAb stuck to a RBC, can also get complement, inflammatory response
-can be mediated by NK cells |
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Term
Explain the mechanism of immediate type 1 hypersensitivity, explain the role of allergens, TH2 helper T cells, IgE secreting plasma cells, mast cells, basophils (circulating mast cells), eosinophils, and release of vasoactive mediators
-immunotherapy |
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Definition
result from the binding of Ag to Ag-specific IgE bound to its Fc receptor (mast cells) -> degranulation -> histamine
IgE mediated, immediate, "allergies," sensitized mast cells
FceRI on mast cells, basophils, eosinophils are cross-linked by Ag binding IgE on cell surface -> degranulation
the chemical mediators released by mast cells attract circulating effector leukocytes (eosinophils, basophils, neutrophils, Th2 cells)
-eos: MBP; cause airway damage in chronic asthma. think chronic
-baso: similar to mast cells, initiate the Th2 response, drives isotype switching to IgE at the beginning of adaptive immune response
-Th2: drive IgE responses
Immunotherapy: antigen desensitization
-gradually i/c conc of dilute Ag over months, specific IgG increases and IgE decreases |
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Term
Differentiate the immediate and late phase of the type 1 hypersensitivity reaction in a person previously sensitized to an allergen
-which cells cause each stage? |
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Definition
immediate: wheal & flare on skin, due to IgE-mediated degranulation of mast cells in skin
-lasts up to 30 min
late-phase rxn: 6-8 hours after immediate rxn
-more widespread swelling
-due to leukotrienes, chemokines, cytokines made by mast cells after IgE activation, not pre-formed |
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Term
| Explain the role of IgE and mast cells in the early response and the prolonged response during an immediate hypersensitivity response |
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Definition
Mast cell activation occurs in the presence of any Ag that can cross-link the IgE molecules bound to FceRI at the cell surface
histamine - rapid response
leukotrienes - 100x more potent, later stages - inflammation, smooth m contraction, airway constriction, secretion of mucus from mucosal epithelium |
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Term
| Describe the action of the mediators released when mast cells degranulate |
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Definition
histamine: vessel permeability, inflammation
chymotryptase, trypase activate metalloproteases that break down EC matrix proteins
TNF-alpha: activates endothelial cells, promote luekocyte entry into tissue
leukotrienes - very potent, later stages
PGD2 - dilation, i/c permeability of BV, chemoattractant for neutrophils (inactivated by aspirin) |
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Term
| Explain immediate type I hypersensitivity as it relates to anaphylactic shock, hives/urticaria, hay fever, allergic rhinitis, asthma, angioedema, food allergies and allergen if introduced intravenously |
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Definition
IV -> systemic anaphylaxis; drugs, serum, venoms, peanuts -> edema, i/c vascular permeability, tracheal occlusion, circulatory collpase, death
SubQ -> wheal & flare; insect bites, allergy testing -> local i/c in blood flow & vascular permeability
-> urticaria
-> (deeper) angioedema
inhaled
-> allergic rhinitis (hay fever); pollens, dust-mite feces -> edema & irritation of nasal mucosa
-> bronchial asthma; pollens, dust mite feces -> bronchial constriction, i/c mucus production, airway inflammation
oral -> food allergy; shellfish, milk, eggs, fish, wheat -> V&D, pruritis (itching), urticaria (hives), anaphylaxis, angioedema |
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Term
Type III hypersensitivity reaction
associated diseases? 2 of them
what type of cells is most likely to respond? |
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Definition
C3a -> histamine -> urticaria
C5a: recruits inflammatory cells
immune complex formation (soluble Ag:IgG-Ab:complement aggregates) deposit in BV walls, alveoli of lungs
beginning of immune response, smaller immune complexes
induce acute inflammatory response
immune complexes activate complement components, attracting neutrophils that contribute to inflammation (degranulation and protease release)
hours to days to develop sx
immune complexes can deposit in skin, kidney (glomerulonephritis), lung and joints: Arthus rxn, serum sicknes
Rheumatoid factor, RA
rash? lupus
a lot of the damage that's done in immune complex formation is by *neutrophils* reacting to Fc portion of Ab |
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Term
| Define an immune complex and their role in the Arthus reaction and serum sickness |
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Definition
Serum sickness: foreign (horse) serum injection, host rejects foreign protein, formation of Ag:Ab complexes (7-10 days) --> fever, vasculitis, arthritis, nephritis, Ab made against foreign serum proteins
-faster response if it's a booster vaccine
-monoclonal Ab, IV penicillin (seen in pts with no hx of allergy to penicillin)
Arthus: usually when vaccinations are given too closely together
-Ab haven't been cleared, 2nd injxn leads to more severe immune response
-locally injected Ag in immune individual with IgG Ab
-local immune-complex formation activates complement, C5a binds to & sensitizes the mast cell to respond
-activation of FcR on mast cells induces degranulation
-swelling, redness, heat, tenderness
Both are type III |
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Term
Know the mechanisms responsible for delayed type hypersensitivity reactions, contact dermatitis and celiac disease (gluten hypersensitivity)
-PPD skin test; will an AIDS pt react? |
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Definition
delayed-type hypersensitivity: insect venom, mycobacterium --> local skin swelling, erythema
contact: haptens (poison ivy, DNFB), small metal ions --> local epidermal rxn (erythema, cellular infiltrate, vesicles, intraepidermal abscesses)
gluten-sensitive: gliadin --> villous atrophy in small bowel, malabsorption
PPD: tuberculin skin test, checking to see if pt has been exposed to mycobacterial TB. If pt has a response, should have T cells, those are what move up into skin and cause a rxn (wheal, flare, etc.)
-*T cell mediated,* usually Th1
-AIDS pt will NOT react, CD4 cells are depleted |
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Term
Define autoimmune diseases and self tolerance
-triggers?
-Auto-Ab mediated
-Auto-Ab mediated with immune complex formation
-T cell-mediated
-Auto-Ab mediated with cellular mechanisms
-molecular mimicry
-immune privilege
-autoimmune hemolytic anemia
-myasthenia gravis
-Grave's
-rheumatoid arthritis
-lupus
-DMTI
-MS |
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Definition
genetics: not necessary or sufficient, but correlated
molecular (antigenic) mimicry: pathogens express regions that resemble self antigens
infection: many viruses & bact induce non-specific B cell activation, leading to auto-Ab formation
trauma: immune privileged sites, inflammation
non-infectious:
-toxins, heavy metals, drugs may alter T cell carrier epitopes to self Ag and render them immunogenic
-hormones-SLE is 10x greater in women, may be exacerbated by estrogen
-loss of T suppressor/regulatory cells
Auto-Ab: Graves', myasthenia gravis, autoimmune hemolytic anemia
Auto-Ab with immune complex formation (type III!): lupus (SLE), rheumatoid arthritis
T cell-mediated: DMTI, MS, rheumatoid arthritis
Auto-Ab mediated with cellular mechanisms: rheumatoid arthritis (neutrophils)
MM:
-streptococcal CW stimulated Ab response (plasma cells, bacteria)
-some Ab cross-react with heart tissue, causing rheumatic fever (immune response to bact produces Ab against epitopes of the bacterial surface; some of these Ab cross-react with heart/others don't)
Immune privilege:
-trauma to one eye results in release of sequestered intraocular protein Ag
-released intraocular Ag are carried to lymph nodes, activate T cells
-effector T cells return via bloodstream, attack Ag in both eyes
Hemolytic anemia: Ab response against RBC
RBC plus anti-RBC autoAb -->
-FcR+ cells in fixed mononuclear phagocytic system --> phagocytosis, RBC destruction
-complement activation and intravascular hemolysis --> lysis, RBC destruction
M. gravis: Ab turns receptor "off"
-normal events at NMJ: Ach receptors, Na+ influx muscle contraction
-M gravis: Ach R internalized & degraded, no Na+ influx/muscle contraction
Grave's: Ab turns receptor "on"
-lose feedback suppression!
-Autoimmune B cell makes Ab against TSH R, stimulates thyroid hormone prod
-thyroid hormones shut down TSH prod but have no effect on autoAb prod, which continues to cause excessive thyroid hormone prod
RA: women 40-60
-Rheumatoid factors: IgM that reacts with Fc of IgG
-rheumatoid IgM binds to normal IgG --> IgM-IgG immune complex
-immune complexes of IgM and anti-IgG against synovial joint Ag
-infiltration of Th1 into joints, release pro-inflammatory cytokines
-joint inflammation, destruction
SLE: women 20-40
-systemic; circulating IgG against cell surfaces, cytoplasm pr & nuclear components
-Ab binds cell surface -> cell destruction
-releases soluble Ag, form immune complexes
-deposit in kidneys, joints, BV
-fever, weakness, arthritis
-kidney damage, butterfly rash
-can be fatal
DMTI: destruction of insulin producing cells in pancreas by self-reactive CD8
-inflammatory cytokine prod, activation of macrophages, production of autoimmune Ab (ctyokines and macrophage lytic enzymes kill beta-islet cells)
-no insulin -> high blood sugar
-seizures, coma
-other common PT
MS: northern hemisphere of West, 20-40 yo
-autoimmune T cell response against myelin sheath of nervous cells (structural proteins of myelin)
-mild numbness to loss of vision, paralysis
-activated Th1
-Th2 may prevent disease
-many tx are beta-IFN that suppress the IR, and mAb against reactive T cells
-Solu-Medrol eases inflammation
-botox? |
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Term
Chronic granulomatous disease
myeloperoxidase deficiency |
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Definition
impaired neutrophil function (NADPH oxidase)
phagocytes can't make O2-, bactericidal activity is reduced
chronic bacterial, fungal & viral infections, granulomas
myeloperoxidase def: similar, less severe PT -> no myeloperox in neutrophil granules, macrophage & lysosomes, impaired production of toxic O2 species -> impaired killing of phagocytosed bacteria -> chronic bacterial, fungal infxns |
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Term
*X-linked hyper IgM
-can cause 2 things |
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Definition
CD40L deficiency
no T-dep B cell activation: isotype switching or somatic hypermutation in B cells
-B cells are present, but T cells aren't working
70% are X-linked
Extracellular (pyogenic) bacterial infxns (no opsonizing IgG)
Absence of germinal centers
still has innate immune response
Tx: gamma globulin
Also causes neutropenia (b/c macrophage activation depends on CD40L) -> mouth sores & blisters
Tx: GM-CSF (stimulates the production & release of phagocytes from BM) |
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Term
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Definition
T cell mutations that, in turn, compromise B cells. *Defect in both cellular and humoral mediated immunity*
50-60% X-linked: Mutation in cytokine receptor chain
The remaining are autosomal recessive, may be a deficit in ADA (adenosine deaminase) causes builds up of derivatives that are toxic to dividing T cells.
Recurrent infections, yeast, bacterial viral.
*Death usually in 1 year, without a bone marrow transplant*
lots of causes:
common gamma chain mutation ("bubble boy")
defects in ADA or PNP
bare lymphocyte syndrome
RAG1 or RAG2
No gene rearrangements in B cells and T cells
susceptible to all types of infection - more severe than B cell def! |
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Term
Bare lymphocyte syndrome
-2 subtypes |
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Definition
TAP1 or TAP2 defect
low MHC I expression, CD8 T cells
SCID not as severe
susceptible to respiratory viral functions
Lack of HLA class II causes SCID
CD4 T cells don't develop, compromises all aspects of adaptive immunity
lack of MHC II products on cells inhibits positive selection of CD4 T cells; Patients still have proper CD8 T cells function. Bone marrow transplant. |
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Term
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Definition
mutation in BtK
B cells blocked at pro-B-cell stage; pts lack antibodies
no BCR, *no mature B cells*
Recurrent bacterial infxns - esp pyogenic encapsulated bacteria (H. influenzae, S. pneumo, S. pyogenes, S. aureus)
Tx: gamma globulin, confers passive immunity, prevents the bronchiectasis that can accompany tx with just antibiotics |
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Term
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Definition
deletion in a gene related to thymic development. Thymic epithelium develops abnormally and T cells fail to develop properly
No CD4 or CD8 T cells, impaired B cell activation.
Loss of T cell immunity, congenital defects of heart, great valves and may have abnormal appearance of mouth eras and face |
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Term
| Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) |
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Definition
absence of AIRE
reduced T-cell tolerance to self Ag
no negative selection in thymus for prevention of autoimmunity
abnormalities of teeth, hair, fingernails |
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Term
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Definition
deficiency in FOXP3
lack of Treg cells & peripheral tolerance
affects mainly boys. gut, thyroid, pancreatic beta cells, skin |
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Term
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Definition
T cells can't signal through their receptors
susceptible to all types of infxn |
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Term
| *selective IgA deficiency* |
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Definition
no major susceptibility
most prevalent among Caucasians
No differentiation of B cells into IgA secreting plasma cells
most common Ig deficiency syndrome |
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Term
IFN-gamma
-what does it do?
-what cells make it, during what immune responses?
-IFN-g receptor deficiency
-*role in graft rejection* |
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Definition
the major cytokine that activates macrophages; esp important against intravesicular bacteria
NK cells during innate response
Th1 CD4 & CD8 T cells during adaptive
IFN-gR def -> persistent mycobacterial infections (homozygous is more severe, although sx are present in hetero)
IFN-g release is initiated by T cells, can up-regulate MHC expression on tissue, provides more targets for mature T cells -> more inflammatory cytokine release
-help by d/c MHC expression |
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Term
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Definition
susceptibility to Neisseria
(no complement-mediated lysis of extracellular bacteria, which requires all components of the complement pathway)
No MAC formation! |
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Term
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Definition
immune complex disease
RBC capture complexes with CR1, which binds to C4b or C3b
this def impairs formation of C4b/C3b
accumulation of immune complexes in blood, lymph, EC fluid & deposition within tissues
activate phagocytes -> inflammation, tissue damage |
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Term
| Leukocyte adhesion deficiency |
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Definition
mutation in CD18 (the beta2 subunit of LFA-1, CR3, CR4)
phagocytes can't migrate to where they're needed
recurrent pygogenic/EC infxns, problems with wound healing |
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Term
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Definition
defects in vesicle fusion of endosomes with lysosomes -> impair intracellular killing by phagocytes
recurrent, persistent bacterial infxn, granulomas, organ effects |
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Term
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Definition
X-linked recessive deficiency of T cell function
-Mutation in a gene that codes for a protein (WASP) that may link membrane receptors to cytoskeletal elements
normal levels of T & B cells, but don't have good Ab responses
thrombocytopenia, eczema, recurrent infxn, early death
Normal thymus initially, but loss of T cells in blood and T cell areas in lymph nodes. No cellular immunity.
Tx: gamma globulin |
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Term
| Why would a pt who received a BM transplant who shared no MHC allotypes with the donor end up with SCID? |
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Definition
the reconstituting T cells selected on the pt's HLA molecules in the thymus couldn't recognize peptide antigens presented by the donor's HLA molecules of the donor-derived APC in the periphery
newly grown T cells raised in the thymus won't recognize antigens presented by APC in the periphery |
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Term
| Describe the process of sensitization to an inhaled allergen. |
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Definition
extraction of Ag by APC
activation of Ag-specific T cells to become Th2 effector cells (secrete IL-4, IL-4 binds B cell, causing B cell to isotype switch & secrete IgE)
production of IgE, binding to mast cells (FceRI)
Second exposure:
-Ag in blood enters tissues, activates mast cells, mast cell degranulation & release of inflammatory mediators (different outcomes in different tissues - i/c vascular permeability, contraction of smooth m, fluid/swelling in tissues) |
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Term
| Common variable immunodeficiency |
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Definition
poorly defined, *B cells are present but cannot differentiate into plasma cells*; hypogammaglobulinemia.
May be related to a deficit in BAFF (B cell survival and differentiation cytokine) receptor |
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Term
|
Definition
failed T and B cell responses due to a lack of TCR or BCR development
Bone marrow transplant |
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Term
what do complement deficiencies lead to?
what are pts more susceptible to? |
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Definition
Leads to impaired humoral immune function and the persistence of immune complexes
*responses will be fast*
Patients with mutations in the classical pathway are more susceptible to *extracellular pathogens due to a lack of clearance of opsonized bacteria* |
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Term
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Definition
hereditary angioedema, swelling due to leakage of fluid from blood vessels into connective tissue, have edema affecting skin and mucosal tissues
C1 inhibitor regulates complement system and protects against “over-activation” via a rise in vasoactive peptides like bradykinin |
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Term
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Definition
Most common, lack early component of classical pathway
Little or no susceptibility to infections (suggesting alternative pathway can handle most infections) but increased incidence of SLE-like autoimmune disease
*impaired clearance of immune complexes* |
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Term
|
Definition
required for both alternative and classical pathways
*serious recurrent pyogenic infections* |
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Term
| how do T cells mediate a Type IV reaction during rheumatoid arthritis? |
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Definition
In affected joints there's leukocyte infiltrate into synovium (CD4 & CD8, B cells, lymphoblasts, plasma cells, neutrophils, macropahges)
-dendritic cells activate CD4 T cells, activate macrophages, secrete pro-inflammatory cytokines & recruit more effector cells
RA: stimulation of B cells that make IgM, IgG, IgA Ab ("rheumatoid factor") specific for FcR of human IgG
Tx: anti-TNF-alpha monoclonal Ab (infliximab) eliminates cytokine; anti-CD20 monoclonal Ab (rituximab) depletes B cells via ADCC |
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Term
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Definition
turns receptor "on"
biased toward a Th2 response
Ab bind to TSH receptor, mimic natural ligand -> chronic overproduction of thyroid hormone independent of TSH regulation
hyperthyroid |
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Term
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Definition
circulating IgG Ab specific for constituents of cell surfaces, cytoplasm, & nucleus
binding -> inflammation -> formation of soluble immune complexes -> deposition in BV, kidneys, joints
butterfly skin rash (erythema) |
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Term
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Definition
autoimmune response against myelin sheath of nerve cells causes sclerotic plaques of demyelinated tissue in CNS white matter
activated Th1 cells & their secreted INF-gamma |
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Term
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Definition
signaling from nerve to muscle across NMJ is impaired
AutoAb bind Ach R on muscle cells, inducing endocytosis. Loss of Ach R makes muscle less sensitive to neuronal stimulation - muscle weakness |
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Term
local vs. generalized anaphylaxis
-what causes death in anaphylactic shock? |
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Definition
caused by degranulation of mast cells or basophils mediated by IgE
localized anaphylaxis (hives, allergic rhinitis, asthma, food allergy)
-only mast cells at site of exposure are degranulated, preformed mediators are short-lived, effects on BV & smooth muscle are limited to immediate vicinity
General (systemic) anaphylaxis: rare, dangerous, can occur within minutes
-allergens have entered the bloodstream -> disseminated mast cell activation
-loss of fluid from BV into tissues --> shock (insufficient BP to supply flow needed to provide O2 to vital tissues)
-death due to asphyxiation due to constriction of the airways & swelling of the epiglottis |
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Term
Why are pts with Ab deficiencies so susceptible to infections involving encapsulated microbes?
-what kind of vaccine can help? |
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Definition
encapsulated microbes aren’t always eliminated by phagocytosis, usually require opsonizing Ab before it can be destroyed
if you don’t have IgG you’re more susceptible
conjugate vaccine, take polysaccharide Ag that’s part of outer capsule, like a toxoid, allows for TI B cell response. T cells responding to the protein carrier can stimulate B cells to make Ab |
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Term
| *What is RhoGAM, what is it used for?* |
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Definition
in Hemolytic Disease (Anemia) of the Newborn: Rh- mother, Rh+ father, baby is Rh+
purified human anti-Rh IgG Ab, given during wk 28 of pregnancy
binds up blood cell Ag that may have been leaked to prevent mother from mounting an immune response against Rh+ blood |
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Term
| Acute rheumatic fever & mimicry |
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Definition
Immune-mediated disease that follows group A streptococcal infection
-Ab develop against group A streptococcal M proteins
-Ab cross-react with similar proteins in human tissue (mimicry)
Occurs at 5 to 15 years of age
Develops over 1 to 5 weeks (average 20 days) after group A streptococcal (Streptococcus pyogenes) pharyngitis |
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