Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
129 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
lymph node
|
- secondary lymphoid organ
- many afferents (entry) - 1 or more efferents (output) - encapsulated - trabeculae |
|
|
|
lymph node functions
|
- non-specific filtration by macrophages
- storage/activation of B and T cells - make antibodies |
|
|
|
follicle
|
- B-cell localization/proliferation
- outer cortex |
|
|
|
primary lymph node follicle
|
- dense and dormant collections of B cells
|
|
|
|
secondary lymph node follicle
|
- B cells with pale, central germinal center
- active |
|
|
|
lymph node MEDULLA
|
- made of medullary cords
- cords = closely packed lymphs + plasma cells - medullary cords + medullary sinuses |
|
|
|
lymph node medullary sinuses
|
communicate with efferent (output) lymphatics
- contain: reticular cells + macrophages |
|
|
|
lymph node paracortex
|
- houses T cells
- between the follicles and the medulla - contains high endothelial venules (T and B cells enter through these from blood) - extreme cellular immune response (viral) = big paracortex - little/small in DiGeorge syndrome |
|
|
|
lymph node drainage:
UPPER LIMB (ARMS) LATERAL BREAST |
AXILLARY NODES
|
|
|
|
node drainage:
STOMACH |
CELIAC NODES
|
|
|
|
node drainage:
DUODENUM JEJUNUM |
SUPERIOR MESENTERIC NODES
|
|
|
|
NODE DRAINAGE:
SIGMOID COLON |
COLIC --> INFERIOR MESENTERIC NODES
|
|
|
|
NODE DRAINAGE:
RECTUM (ABOVE PECTINATE LINE) |
INTERNAL ILIAC NODES
|
|
|
|
NODE DRAINAGE:
ANAL CANAL BELOW PECTINATE LINE |
SUPERFICIAL INGUINAL PECTINATE LINE
|
|
|
|
TESTES NODE DRAINAGE
|
SUPERFICIAL AND DEEP PLEXUSES --> PARA-AORTIC NODES
|
|
|
|
NODE DRAINAGE:
SCROTUM |
SUPERFICIAL INGUINAL
|
|
|
|
NODE DRAINAGE:
THIGH (SUPERFICIAL) |
SUPERFICIAL INGUINAL NODES
|
|
|
|
NODE DRAINAGE:
LATERAL SIDE OF DORSUM OF FOOT |
POPLITEAL NODES
|
|
|
|
RIGHT LYMPHATIC DUCT
|
DRAINS RIGHT ARM AND RIGHT 1/2 OF HEAD
|
|
|
|
THORACIC DUCT
|
DRAINS EVERYTHING ELSE
|
|
|
|
SPLEEN SINUSOIDS
|
- long, vascular channels in red pulp
- fenestrated "barrel hoop" BM - macrophages are nearby |
|
|
|
SPLEEN SINUSOIDS
|
T cells are in periarterial lymphatic sheath (PALS) and in white pulp of spleen
|
|
|
|
SPLEEN SINUSOIDS
|
B cells are in follicles in the white pulp of the spleen
|
|
|
|
SPLEEN SINUSOIDS
|
macrophages here remove bacteria with capsules
|
|
|
|
SPLENIC DYSFUNCTION
|
dec. IgM -> dec. activation of C'
-> dec. C3b opsonization leading to inc. susceptibility to capsuled organisms |
|
|
|
ENCAPSULATED ORGANISMS
|
"S SHiN"
Salmonella S. pneumoniae H. influenzae N. meningitidis |
|
|
|
POSTSPLENECTOMY
|
Ho-Jo bodies (remnants of nuclei)
target cells high plts (thrombocytosis) |
|
|
|
THYMUS
|
site of T cell differentiation/maturation
|
|
|
|
THYMUS
|
- capsule surrounds it
- origin = epithelium of 3rd branchial pouch |
|
|
|
THYMUS
|
lymphocytes of mesenchymal origin
|
|
|
|
THYMUS CORTEX
|
- lots of immature T cells
|
|
|
|
THYMUS MEDULLA
|
- pale
- mature T cells + epithelial reticular cells - Hassall's corpuscles |
|
|
|
Hassall's corpuscles
|
dead, type VI reticular epithelial cells (concentric epithelial cells that contain keratohyaline granules)
- probably left over from ectoderm from nearby 3rd arch during embryogenesis |
|
|
|
THYMUS CORTICOMEDULLARY JUNCTION
|
- where positive and negative selection happen
|
|
|
|
POSITIVE THYMIC SELECTION OF T CELLS
|
MHC restriction
|
|
|
|
NEGATIVE THYMIC SELECTION OF T CELLS
|
ensure that T cells don't react with self antigens
|
|
|
|
T vs B cell maturation
|
T cells = Thymus
B cells = Bone marrow |
|
|
|
INNATE IMMUNITY
|
germline codes for receptors that recognize pathogens
|
|
|
|
INNATE IMMUNITY
|
no memory is involved
|
|
|
|
INNATE IMMUNITY
|
consists of:
- SEGs - macrophages - dendritic cells - NK cells (lymphoid origin) - C' |
|
|
|
ADAPTIVE IMMUNITY
|
- receptors undergo V(D)J recombination in order to recognize pathogens during lymphocyte development
|
|
|
|
ADAPTIVE IMMUNITY
|
- first exposure to antigen = slow response
- memory response = stronger and faster |
|
|
|
ADAPTIVE IMMUNITY
|
made of:
- T cells - B cells - circulating antibodies |
|
|
|
MHC
|
- major histocompatibility complex
- coded for by HLA genes - used to present pieces of antigens to T cells and mechanisms to bind TCR's |
|
|
|
MHC-I
|
HLA-A
HLA-B HLA-C |
|
|
|
MHC-I
|
- expressed on all cells with nucleus (not rbc's)
- antigen is loaded onto the MHC in the RER - mediates immunity to viruses - paired with beta2-microglobulin = helps get MHC-I/antigen to surface of cell - ***BINDS TCR and CD8+ cells (CTL) - 1 chain + beta2-microglobulin |
|
|
|
MHC-II
|
HLA-DR
HLA-DP HLA-DQ |
|
|
|
MHC-II
|
- only on antigen presenting cells
- antigen is broken down in acidified endosome - invariant chain is released from endosome - ***BINDS TCR and CD4+ - 2 chains = alpha and beta |
|
|
|
HLA-A3
|
hemochromotosis
|
|
|
|
HLA-B27
|
PAIR
- Psoriasis - Ankylosing spondylitis - IBD - Reiter's syndrome |
- Psoriasis
- Ankylosing spondylitis - IBD - Reiter's syndrome |
|
|
HLA-B8
|
Graves' disease
|
|
|
|
HLA-DR2
|
- MS
- hay fever - SLE - Goodpasture's |
|
|
|
HLA-DR3
|
- DM I
|
|
|
|
HLA-DR4
|
- RA
- DM I |
|
|
|
HLA-DR5
|
- pernicious anemia (B12 deficiency)
- Hashimoto's thyroiditis |
|
|
|
HLA-DR7
|
- steroid-responsive nephrotic syndrome
|
|
|
|
NK cells
|
- induce apoptosis of infected/tumor cells
- use PERFORIN + GRANZYMES |
|
|
|
NK cells
|
only lymphocyte that's part of innate immunity
|
|
|
|
NK cells
|
inc. activity of NK cells with:
- IL-12 - IFN-β - IFN- α |
|
|
|
NK cells
|
- induced to kill a cell when:
- non-specific activation signal is attached to target cell - OR - there is no MHC-I on the surface of the target cell |
|
|
|
B-CELL FUNCTION
|
- make antibody
|
|
|
|
ANTIBODY FUNCTION
|
- opsonize bacteria
- IgG = neutralize viruses - IgG, IgM = activate C' - IgE = sensitize mast cells |
|
|
|
B-CELL FUNCTION
|
- make IgE = type I hypersensitivity = allergy
- type II hypersensitivity = cytotoxic - type III hypersensitivity = immune complex (both II and III are IgG) |
|
|
|
B-cell function
|
hyperacute rejection of organ
(mediated by antibodies) |
|
|
|
T cell function
|
CD4+ T cells
- help B cells make antibody - make IFN = stimulate macrophages |
|
|
|
T cell function
|
CD8+ T cells
- directly kill virus infected cells |
|
|
|
T cell function
|
DTH (delayed type hypersensitivity)
|
|
|
|
T cell function
|
acute and chronic rejection of organ
|
|
|
|
T cell differentiation
|
- in bone marrow = T cell precursors with no receptors
|
|
|
|
T cell differentiation
|
precursor from BM to thymus:
- here, have CD4, CD8 and TCR's on surface |
|
|
|
T cell differentiation = CORTEX (positive selection)
|
- determines whether T cells will be CD8 or CD4 + cells
|
|
|
|
T cell differentiation = MEDULLA (negative selection)
|
- does it react to self antigens?
if yes = apoptosis if no = circulates to lymph node |
|
|
|
T cells in nodes
|
cytotoxic/CD8+ T cells kill:
- virus infected - neoplastic - donor graft cells |
|
|
|
T cells in nodes
|
helper/CD4+ T cells:
Th1 cells: - cell-mediated response Th2 cells: - humoral/antibody response |
|
|
|
T and B cell activation
|
need 2 signals to activate T cells and cause Ab class switching in B cells
|
|
|
|
Th activation
|
1) APC eats foreign body
2) present antigen on MHC II - Th cell's TCR recognizes MHC II + antigen on APC = signal 1 3) B7 and CD28 bind = "co-stimulatory signal" = signal 2 4) Th is activated and starts making cytokines |
|
|
|
CTL activation
|
1) viral or self proteins inside the virally infected cells attached to MHC-I and presented on surface
- TCR on the CTL recognizes the MHC-I = signal 1 2) Th cell makes IL-2 - IL-2 activates the CTL = kill virus-infected cells = signal 2 |
|
|
|
B-CELL CLASS SWITCHING
|
1) Th2 cell makes IL-4, IL-5, IL-6 = signal 1
2) B cell has CD40 receptor that binds to CD40L on the Th cell = signal 2 |
|
|
|
Th1 cell
|
- regulates cell-mediated response
- makes Th1 cytokines = IL-2, IFN-γ |
|
|
|
Th1 cells
|
activate:
- CTL/CD8+ T cells - macrophages |
|
|
|
Th1 cells
|
inhibited/down regulated by:
- IL-10 (made by Th2 cells) |
|
|
|
Th2 cells
|
- regulate antibody/humoral response
|
|
|
|
Th2 cell cytokines
|
IL-4
IL-5 IL-10 |
|
|
|
Th2 cell
|
helps B cells make antibodies
- IgE > IgG |
|
|
|
Th2 cells
|
inhibited by:
- IFN-γ from Th1 cells |
|
|
|
macrophage-lymphocyte interaction
|
- activated lymphocytes make/release IFN-γ
- macrophages make/release IL-1 + TNFα - stimulate each other |
|
|
|
Th cells
|
CD4+ = binds to MHC II on APCs
|
|
|
|
CTL
|
kill:
- virus infected - neoplastic - donor graft cells induce apoptosis |
|
|
|
CTL = induce apoptosis
|
release cytotoxic granules with proteins:
- perforin = makes hole in cell membrane - granzyme = serine protease; activates apoptosis inside cell - granulysin = antimicrobial, induces apoptosis |
|
|
|
CTL
|
CD8+ = binds to MHC I on virus-infected cells
|
|
|
|
ANTIBODIES
|
- variable light and heavy chain regions recognize antigens
|
|
|
|
ANTIBODIES
|
Fc fragment of IgG and IgM = fixes C'
|
|
|
|
HEAVY AND LIGHT CHAINS
|
heavy = part of Fab and Fc
light = only Fab |
|
|
|
Fab fragment of antibodies
|
- bind to the antigen
- determines the idiotype = unique antigen-binding pocket - each B cells is specific for just one specific antigen |
|
|
|
Fc fragment
|
- constant region
- Carboxy terminal - Complement binds at the middle region of Fc fragment = Ch2 (only for IgG and IgM) - Carb side chains - determines isotype (is it IgM, IgD, etc.) |
|
|
|
GENERATION OF SPECIFIC/DIVERSE ANTIBODIES
|
1)- light chain = VJ gene recombination
- heavy chain = V(D)J gene recombination 2) random combinations of heavy and light chains 3) after antigen stimulation = somatic hypermutation 4) tdt (terminal deoxynucleotide transferase) adds nucleotides to DNA during recombination |
|
|
|
OPSONIZATION
|
antibody binds to foreign body to help phagocytes recognize it
|
|
|
|
NEUTRALIZATION
|
antibodies binds to stop bacteria from binding to cells (like in GI tract) = prevents entry
|
|
|
|
COMPLEMENT ACTIVATION
|
antibody provides a place for C' to bind = helps C' do its job = opsonization + lysis of bacterium
- esp. C3b and the MAC |
|
|
|
Ig Isotypes
|
- mature B lymphs show IgM and IgD on surface
- differentiate by switching isotypes via alternative DNA splicing of mRNA) - mediated by cytokines + CD40L - become plasma cells that secrete IgA, IgE or IgG |
|
|
|
IgG
|
- #1 antibody in secondary/delayed antigen response
- greatest amount in blood - fixes/binds C' - crosses placenta (gives babies passive immunity = they didn't do anything to get it) - opsonizes bacteria - neutralizes bacterial toxins/viruses |
|
|
|
IgA
|
- stops bacteria/viruses from binding to mucous membranes
- doesn't fix C' - circulating IgA = monomer - secreted IgA = dimer - crosses epithelial cells via transcytosis - secreted into tears, saliva, mucus, breast milk (colostrum) - acquires secretory part from epithelial cells before secretion |
|
|
|
IgM
|
- made in the primary/immediate response to antigen
- binds/fixes C' - doesn't cross placenta - on the surface of B cells and acts like a receptor = monomer - circulating IgM = pentamer - shape of pentamer = catch free antigens while antibodies are being induced and made |
|
|
|
IgD
|
- don't know function
- in the serum + on surface of B cells |
|
|
|
IgE
|
- binds to mast cells + basophils
- when exposed to allergen, cross-links (attached to cells) - mediate type I hypersensitivity - induces release of inflammatory mediates (histamine) - immunity to worms (activate eo's) - lowest concentration in serum |
|
|
|
thymus-independent antigens
|
- antigens w/o peptide part = they can't be presented on MHC to T cells
- example = LPS from GN bacteria, polysaccharide capsular antigen - induces release of IgM only - don't produce memory B cells (b/c don't activate T cells) |
|
|
|
thymus-dependent antigens
|
- antigens that have a protein part
- example = conjugated H. influenzae vaccine - get class switching and memory b/c directly contact B cells with Th cell (via CD40 - CD40L interaction) - induces release of IL-4, IL-5, IL-6 |
|
|
|
COMPLEMENT
|
- system of proteins
- interact with each other in humoral/antibody mediated immunity and inflammation |
|
|
|
COMPLEMENT
|
- MAC = against GN bacteria
- classic pathway (antigen-antibody) = activated by IgG or IgM - alternative pathway = activated by molecules on surface of bacteria (esp. endotoxins) |
|
|
|
complement
|
- C3b + IgG = #1 in defense against bacteria
- C3b = helps clear immune complexes |
|
|
|
COMPLEMENT
|
- DAF = decay-accelerating factor + C1 esterase inhibitor = prevent activation of C' on self-cells
|
|
|
|
ALTERNATIVE PATHWAY ACTIVATION OF COMPLEMENT
|
- non-specific molecules/microbial surfaces/endotoxin = binds C3 with water + B + D
- leads to C3b, Bb; C3 convertase converts to C3 - C3a binds to C3b,Bb,C3b - C5 convertase activates C5 then common pathway |
|
|
|
LECTIN ON MICROBIAL SURFACES (MBL)
|
- C' binds here and protease cleaves C2 and C4
- C4b, 2b via C3 convertase activates C3 - C3a + C4b,2a,3b with C5 convertase activate C5 and then continue in common pathway |
|
|
|
CLASSIC (ANTIGEN-ANTIBODY) PATHWAY OF COMPLEMENT ACTIVATION
|
- C1 is activated and then activates C2 and C4 and continues same pathway as MBL stimulation
- "GM makes CLASSIC cars" |
|
|
|
COMMON PATHWAY
|
- C5 bound to C5a+MC5b
- add C7 and C6 = MC5b,6,7 - add C8 and C9 = MC5B,6,7,8,9 = MAC --> lysis, cytotoxicity |
|
|
|
C1,2,3,4
|
neutralize viruses
|
|
|
|
C3b
|
B = binds bacteria
- opsonization |
|
|
|
C3a, C5a
|
A = anaphylaxis
|
|
|
|
C5a
|
attracts neutrophils
|
|
|
|
C5b,6,7,8,9 = MAC
|
- causes cytolysis via the MAC
|
|
|
|
C1 esterase inhibitor deficiency
|
- not enough inhibition of C1 esterase
- C1 esterase inhibitor stops C' from binding to self cells - leads to HEREDITARY ANGIOEDEMA |
|
|
|
C3 DEFICIENCY
|
- severe, recurrent pyogenic sinus and respiratory tract infections
- more susceptible to type III hypersensitivity reactions (immune complex related) |
|
|
|
C5-C8 DEFICIENCY
|
leads to Neisseria bacteremia
|
|
|
|
DAF DEFICIENCY (GPI-anchored enzyme)
|
- leads to C'mediated lysis of rbcs = PNH paroxysmal nocturnal hemoglobinuria
|
|
|
|
CYTOKINES SECRETED BY MACROPHAGES
|
IL-1
IL-6 IL-8 IL-12 TNFalpha |
|
|
|
IL-1
|
-secreted by macrophages
- endogenous pyrogen - causes fever + acute inflammation - causes endothelium to put out adhesion molecules - induces secretion of chemokines to attract WBCs |
|
|
|
IL-6
|
- endogenous pyrogen
- secreted by Th cells too - causes fever - induces production of acute phase proteins |
|
|
|
IL-8
|
#1 chemotactic factors for SEGs
|
|
|
|
IL-12
|
induces differentiation of Th cells into Th1 cells
- activates NK cells - secreted by B cells too |
|
