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74 Cards in this Set

  • Front
  • Back
Innate immunity
Receptors that recognize pathogens are germline encoded; response to pathogens is fast and nonspecific. No memory
Adaptive immunity
Receptors that recognize pathogens undergo VDJ recombination during lymphocyte development. Response is slow to first exposure, but memory response is faster and more robust
found on all nucleated cells; binds to CD8
viral immunity
found only on APCs
main antibody in secondary response; most abundant; fixes complement, crosses placenta, opsonizes bacteria, neutralizes bacterial toxins and viruses; half life is 21 days
prevents attachment of bacteria and viruses to mucous membranes; does not fix complement; monomer or dimer; found in secretions
Produced in primary response to an antigen; fixes complement but does not cross the placenta; on B cells; monomer or pentamer
found on surface of B cells
mediates type I HS- induces release of mediators from mast cells and basophils when exposed to allergen
mediates immunity to worms
secreted by macrophages; stimulates T and B cells, neutropils, fibroblasts and epithelial cells to grow, differentiate or synthesize specific proteins
secreted by Th1 cells; stimulates growth of helper and cytotoxic T cells
secreted by activated T cells; supports the growth and differentiation of bone marrow stem cells; has function similar to GM-CSF
secreted by Th2 cells; promotes growth of B cells; makes IgE and IgG
secreted by Th2 cells; promotes differentiation of B cells; makes IgA; stimulates production and activation of eosinophils
secreted by Th cells and macrophages; stimulates production of acute phase reactants and immunoglobulins
major chemotactic factor for neutrophils (along with C5a)
secreted by Th2 cells. stimulates Th2 while inhibiting Th1
secreted by B cells and macrophages. Activates NK and Th1 production
gamma IFN
secreted by Th1 cells, stimulates macrophages
secreted by macrophages; increases IL2 receptor synthesis by Th cells; increases B cell proliferation, attracts and activates neutrophils; stimulates dendritic cell migration to LN
Acute phase reactants
IL1, IL6, TNF alpha
Th1 cell
induced to form by IL12; produce IL2, IFN IL12, and activates macrophages and CD8 cell (cytotoxic T)
Th2 cell
induced to form by IL4; produce IL4, IL5, IL10 and help B cells make antibody
Helper T cell surface proteins
CD4, TCR, CD3, CD28, CD40L
Cytotoxic T cells surface proteins
B cells surface proteins
IgM, IgD, B7, CD19, CD20, CD40, MHCII, CD21
Macrophage surface proteins
MHCII, CD14, Receptors for Fc and C3b, CD16
NK cells
receptors for MHCI, CD16, CD56
Decay accelerating factor
CD55, 59- on wbc, rbc, and platelets, protect against complement damage
Alternative complement pathway stimulated by
microbial surfaces
Lectin pathway stimulated by
microbial surfaces
Classic pathway stimulated by
antigen-antibody complexes
C1, C2, C3, C4
viral neutralization
C3a, C5a
neutrophil chemotaxis
cytolysis by MAC
Def of C1 estarase inhibitor
hereditary angioedema
Def of C3
severe recurrent pyogenic sinus and respiratory tract infections
Def C6-C8
Neisseria bacteremia
Def of DAF
paroxysmal nocturnal hemoglobinuria
dx with HAMS (RBC lysis at low ph) or flow cytometry for CD55, 59
What do IFNs do
induce the production of a second protein that inhibits viral protein synthesis by degrading viral mRNA; also activate NK cells to kill virus infected cells
alpha and beta IFN
inhibit viral protein synthesis
gamma IFN
increase MHC I and II expression and antigen presentation in all cells
Active immunity
induced after exposure to foreign antigens; slow onset; long lasting protection
Passive immunity
based on receiving preformed antibodies from another host; rapid onset; short life span of antibodies
Give passive immunity for
Tetanus, Botulinum, HBV, Rabies, RSV exposure
Type I HS
antigen cross links IgE on presenstized mast cells, triggering release of vasoactive amines; RAPID
Type II HS
antibodies against self- IgM, IgG bind to antigen leading to lysis by complement or phagocytosis
Immune complex mediated; deposit in tissues and activate immune system
Type IV HS
delayed type- sensitized T lymphocytes encounter antigen and then release lymphokines- leads to macrophage activation
Type I HS examples
anaphylaxis, allergic rhinitis, asthma, hives
Type II HS examples
hemolytic anemia, Idiopathic TCP, erythroblastosis fetalis, rheumatic fever, goodpastures, bullous pemphigoid, graves, myasthenia gravis
Type III HS examples
lupus, RA, polyarteritis nodosum, PSGN, serum sickness, arthus reaction, HS pneumonitis
Type IV HS examples
T1DM, MS, Guillain Barre, Hashimotos, GVHD, PPD, contact dermatitis
Psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease, reiter's syndrome
hyper acute rejection
antibody mediated due to the presence of preformed antibodies on donor; immediate
acute rejection
cell mediated due to cytotoxic T lymphos reacting against foreign MHCs; occurs weeks after; reversible
chronic rejection
antibody mediated vascular damage; months to years after; irreversible
T cells mediated; bone marrow graft has new immune system that attacks the host
displayed only by helper T cells
displayed only by cytotoxic T cells
found on all T cells (except NK)
used to ID B cells
CD19, 20, 21
Bruton's agammaglobulinemia
X linked (boys), B cell def- defective tyrosine kinase gene
low levels of ALL Igs
recurrent bacterial infections after 6 mos
Thymic aplasia (DiGeorge)
3rd and 4th pouches fail to develop- no thymus - no T cells, no PTH - low Ca, tetany
congenital defects in heart and great vessels, recurrent viral, fungal and protozoal infections
22q11 deletion
Chronic mucocutaneous candidiasis
T cell dysfunction against C albicans
adenosine deaminase deficiency; recurrent infections
Wiskott Aldrich Immunodeficiency
TCP, eczema, recurrent pyogenic infections, no IgM vs capsular bacteria, high IgA
X linked
Ataxia telangiectasia
IgA def; cerebellar ataxia; spider angiomas
Selective Ig def
IgA is most common, usually asymptomatic
Chronic granulomatous disease
lack of NADPH oxidase activity- impotent phagocytes
opportunistic infections- S aureus, E Coli, Aspergillus
prophylactic TMP-SMX
Chediak Hegashi
defective macrophages- microtubular and lysosomal
see giant granules in neutrophils
recurrent staph/streph infections
partial albinism
Job's sydrome
no Th cell production of IFN gamma; neutrophils fail to respond to chemotactic stimuli
high levels of IgE
recurrent staph abscesses