Immunology Exam 2

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alternative complement activation pathway

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microbial cell walls, basement membranes

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lectin complement activation pathway

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collections: C-reactive protein, mannan-binding lectin

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classical complement activation pathway

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IgG >> IgM antibodies bound to antigen

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complements involved in mast cell activation

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C3a, C5a

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complements involved in chemotaxis

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C5a

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complements involved in opsonization

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C3b

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complements involved in enhancing antibody production

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C3b

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complements involved in microbial killing

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MAC = C5b678(9n)

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C3a

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mast cell activation

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C3b

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enhance Ab production
opsonization

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C5a

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mast cell activation
chemotaxis

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C5b678(9n)

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microbial killing (pore formation)

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hematopoeitic cytokines

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G-CSF

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inflammatory cytokines

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IL-1, IL-6, TNF-alpha, IFN-gamma

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antiviral cytokines

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IFN-alpha, IFN-beta, IFN-omega (IFN-gamma)

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immunologic cytokines

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IL-2, IL-4, IL-5, IFN-gamma (pro)
IL-10, TNF-beta (anti)

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G-CSF

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hematopoetic cytokine
released by macrophages
promotes neutrophil production in bone marrow

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IL-1

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inflammatory cytokine
released by macrophages and mast cells
induce acute-phase response
promote adhesion of leukocyte to vessel walls

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IL-6

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pro-inflammatory cytokine
released by macrophages++
induce acute-phase response

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TNF-alpha

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pro-inflammatory cytokine
released by macrophages and mast cells
induce acute-phase response
promote adhesion of leukocyte to vessel walls

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IFN-alpha

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antiviral cytokine
released by most cells
promote adaptive immunity

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IFN-beta

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antiviral cytokine
released by most cells
promote adaptive immunity

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IFN-omega

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antiviral cytokine
released by most cells
promote adaptive immunity

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IFN-gamma

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antiviral, proinflammatory, immunologic
released by Th1 and NK cells
activates macrophages (to release NO)

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IL-2

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immunologic
released by Th1
promotes T lymphocyte proliferation

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IL-4

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immunologic cytokine
released by Th2
promotes IgE secretion by B lymphocytes

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IL-5

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immunologic cytokine
released by Th2
recruits and activates eosinophils

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IL-10

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anti-inflammatory cytokine
released by Treg cells
inhibit inflammatory and adaptive immune response

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TGF-beta

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anti-inflammatory cytokine
released by Treg cells
inhibit inflammatory and adaptive immune reponse

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essential functions of inflammation

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--dilute and remove injurious agent and any tissue debris from site of injury
--prepare tissue for repair and healing

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3 microvascular processes in acute inflammation

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--vasodilation of arterioles
--increased vascular permeability of capillaries and venules
--leukocyte emigration through venules

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chemical mediators of vasodilation

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serotonin, histamine, prostaglandin E2
acts to increase blood flow to site of infection

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chemical mediators of increased vascular permeability

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histamine and serotonin
acts to recruit antimicrobial plasma proteins (i.e. complement, Abs) to site of infection

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chemical mediators of leukocyte emigration

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adhesion: IL-1, TNF-alpha
chemotaxis: chemokines, C5a, leukotriene B4, bacterial peptides
acts to recruit phagocytes to site of infection

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virus PAMPs

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cytoplasmic RNA, dsRNA, certain sequences viral RNA, certain viral proteins

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bacterial PAMPs

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lipopolysaccharides (LPS), peptidoglycan, certain sequences of bacterial DNA, surface mannose and other sugars, flagella

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fungal PAMPs

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surface mannose and other sugars, chitin

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sentinel cells

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epithelial cells, macrophages, dendritic cells, mast cells

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histamine

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vasodilation, increased vascular permeability (adhesion of leukocytes at vessel walls)
released by mast cells
inhibited by antihistamines, glucocorticoids

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serotonin

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vasodilation, increased vsacular permeability (adhesion of leukocytes to vessel walls)
released by mast cells
inhibited by glucocorticoids

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prostaglandin E2

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vasodilation
released by mast cells and macrophages
inhibited by glucocorticoids and NSAIDs

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chemokines

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subset of cytokines that act as chemotactic factors to recruit leukocytes to site of infection
inhibited by glucocorticoids
released by many cells

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leukotriene B4

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chemotaxis (recruitment of leukocytes to site of infection)
released by mast cells and macrophages
inhibited by some NSAIDs and glucocorticoids

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bacterial peptides

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chemotaxis function
released by bacteria
not inhibited?

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what mediators of inflammation do glucocorticoids inhibit?

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serotonin, histamine, prostaglandin E2, chemokines, leukotriene B4

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what mediators of inflammation do NSAIDs inhibit?

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prostaglandin E2, leukotriene B4

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what cytokines initiate the acute-phase responses?

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IL-1, IL-6, TNF-alpha (pro-inflammatory cytokines)

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functions of acute-phase proteins

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amplify host defenses: recognize PAMPs (complement activation and opsonization), microbial killing, regulate host defenses (limit inflammation)
assist in tissue repair (fibrin)

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identifying surface molecules of B lymphocytes

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CD79a and CD79b
mIg = BCR
MHC class II

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identifying surface molecules of T lymphocytes

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CD3
CD4 or CD8
TCR (alpha-beta or gamma-delta)

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primary lymphoid tissues

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bone marrow
thymus
Cloacal bursa, ileal Peyer's patches

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secondary lymphoid tissues

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spleen, MALT, lymph node

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MALT

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Mucosal Associate Lymphoid Tissues
intraepithelial lymphocytes, jejunal Peyer's patches, lamina propria, basal lamina

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gene segments involved in combinatorial selection of genes during lymphocyte maturation

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V = variable
D = diversity
J = joining

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SCID

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inherited immunodeficiency in Arabian foals
inability to splice chromosomes together
unable to make Ag receptors --> no T or B lymphocytes

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MHC Class I

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expressed by all nucleated cells
presents to CD8 T cells
Ags: viral Ags, intracellular parasites

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Ag processing in MHC Class I

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acquistion: synthesized in cell
fragmentation: proteosome
MHC binding: ER
transport: via Golgi

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MHC Class II

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expressed by DCs, macrophages, B lymphocytes
presents to CD4 T cells
Ags: extracellular parasites, extracellular phase of intracellular parasites

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Ag processing in MHC Class II

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acquisition: endocytosis
fragmentation: endosome (enzymes and acidification)
MHC binding: endosome
transport: direct to membrane

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Myeloid DCs

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found in most tissues, diffuse cortex of LNs, spleen, thymus
capture and process Ags to present to T lymphocytes

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Follicular DCs

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found in lymphoid nodules/follices
capture and present Ags to B lymphocytes

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Plastacytoid DCs

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found in blood and lymphoid tissues
secrete IFN-alpha and IFN-beta (antiviral cytokines)

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anergy

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state of inactivation that occurs when an immature myeloid DC presents Ag to T cell but without the activation signal --> no immune response

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positive selection of T lymphocytes

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T lymphocyte recognizes MHC Class I --> CD8
T lymphocyte recognizes MHC Class II --> CD4
T lymphocyte doesn't recognize a MHC --> apoptosis

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negative selection of T lymphocytes

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CD4/CD8 binds mod affinity to self Ag --> maturity
CD8 binds hi affinity to self Ag --> apoptosis
CD4 binds hi affinity to self Ag --> apoptosis OR Treg cell

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what are 2 ways to initiate an immune response?

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--in secondary lymphoid tissues
--myeloid DCs present Ag to and activate CD4 T cells

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myeloid DC activation process

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1. acquire Ag: phagocytosis, pinocytosis, receptor-mediated endocytosis
2. maturation signal: PAMPs, DAMPs, inflammatory cytokines (express B7)
3. migrate to LN
4. present to T cells

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recognition signal of B lymphocytes

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Ag (binds to mIg and is internalized)

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activation signal of B lymphocytes

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Tfh cells (B cell presents Ag to Tfh cell with MHC Class II --> Tfh expresses CD40L to deliver activation signal)

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proliferation of B lymphocytes

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Tfh cytokines
occurs in secondary lymphoid follicle with germinal center
class switching
somatic hypermutation

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differentiation of B lymphocytes

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plasma cells --> secrete Abs
memory cells --> circulate back to origin tissue and act in amanestic response

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recognition signal of CD4 T lymphocytes

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MHC Class II and Ag

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recognition signal of CD8 T lymphocytes

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MHC Class I and Ag

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activation signal of CD4 T lymphocytes

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Dendritic Cells (mature myeloid DCs express B7 membrane receptor and deliver Ag in MHC)

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activation signal of CD8 T lymphocytes

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Dendritic cells (mature myeloid DCs express B7 membrane receptor and deliver Ag in MHC) and cytokines from Th1

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proliferation factor of T lymphocytes

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IL-2 (Secreted by Th1)

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Class switching of B lymphocytes

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immature B lymphocytes first express IgM as BCR
during proliferation, B cells switch classes via chromosome splicing
sam Ag specificity, but different classes of Ig

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Somatic hypermutation of B lymphocytes

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during proliferation, By cells accumulate mutations in variable region to change (+/-) affinity for Ag
affinity maturation (increased strength of binding, not specificity)

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what are differences between primary and secondary immune responses?

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secondary response is faster and greater in magnitude
1: IgM first; 2: more IgG and IgA
increased affinity of B binding (not true of TCR)

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how is an immune response terminated?

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--Ag elimination
--IgG bounds to Ag inhibits B cell activation
--Treg cells

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heavy chain of Ig

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2 present (alpha, delta, gamma, mu)
1 variable domain, 3 constant domains

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light chain of Ig

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2 present (identical)
either kappa or lambda
1 variable domain, 1 constant domain

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Fab region of IgG

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includes variable and constant domains of light and heavy chains
binds Ag
not crystallizable

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Fc region of Ig

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includes constant domains of heavy chains
determines function, no Ag binding
crystallizable

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IgG structure

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gamma heavy chain; monomer
high plasma conc.
made in systemic immune system
found in plasma and tissue fluids

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IgM structure

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mu heavy chain
BCR as monomer; secreted as pentamer
lower plasma conc.
made in systemic immune system and MALT
found in plasma

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IgA structure

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alpha heavy chain; J chain; secretory component
BCR as monomer; secreted as dimer
lower plasma conc.
made in MALT
found in secreteions and plasma

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IgE structure

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epsilon heavy chain; monomer
very low in plasma
made in MALT
associated with mast cells

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5 functions of immunoglobulins

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neutralization, complement activation, opsonization, ADCC, mast cell activation

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Ig: neutralization

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inhibition by binding and preventing attachment to cellular receptors
IgG, IgM, IgA

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Ig: complement activation

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initiates classical pathway of complement activation via binding to C1
IgM >> IgG

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Ig: opsonization

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Fab binds to infectious agent; Fc binds to phagocytes
IgG >> IgA, IgM

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Ig: Antibody-Dependent Cellular Cytotoxicity

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Ig binds to large pathogen; phagocyte binds to Fc and releases enzymes
IgG; IgE with eosinophils

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Ig: mast cell activation

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IgE binds to Fc receptors on mast cells and triggers degranulation

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IgG functions

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neutralization, complement activation (limited), opsonization, ADCC (neutrophils, macrophages, NK cells, eosinophils)

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IgM functions

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neutralization, complement activation, limited opsonization

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IgA functions

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neutralization, limited opsonization

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IgE functions

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ADCC with eosinophils, mast cell activation

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function of CD8 T lymphocytes

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Cytotoxicity ("killers")
release granules --> form membrane pore --> send proteins in to signal apoptosis

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function of Th1 lymphocytes

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Macrophage recruitment and activation
secrete IL-gamma to activate macrophages to produce NO
secrete IL-2 for T lymphocyte proliferation

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function of Th2 lymphocytes

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Eosinophil recruitment and activation
secrete IL-4 to promote IgE synthesis by B cells
secrete IL-5 to recruit and activate eosinophils

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function of Th17 lymphocytes

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Neutrophil activation and recruitment
secrete IL-17
activate fibroblasts and epithelial cells --> release cytokines --> recruit neutrophils into tissues
fibroblasts --> release G-CSF --> increase bone marrow synthesis of neutrophils

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function of Tfh lymphocytes

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B lymphocyte activation
secrete cytokines necessary to activate B lymphocytes that present a recognizable Ag

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function of Treg lymphocytes

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secrete IL-10 and TGF-beta to suppress immune response
secrete adenosine
direct contact for inhibition of immune response