chapter 22- lymphatic system and immunity Flashcards
when a hemocytoblast produces what stem cells, T cells, B cells & NK cells will be created
lymphoid
T cells get their name for the fact that they mature in what organ?
thymus
what makes a lymphoid organ unique from a lymphoid follicle/nodule?
organ has a capsule
the middle of a lymphoid follicle is the what & is where B cells are dividing
geminal center
the collective term for all the lymphoid nodules along the intestine is the MALT
which stands for what?
mucosa-associated lymphoid tissue
There are 2 what tonsils visible at the back of the mouth?
palatine
lymph enters a lymph node through many what vessels and then slowly filters through the sinuses?
afferent
the red pulp of the spleen is made up of what filled with blood?
sinusoids
the cutaneous membrane is protective against microbes due to the thick keratin,
acid & what else?
salt
what is the enzyme produced in mucus secretions specifically
disrupt the walls of bacterial cells?
lysozyme
neutrophils secrete what which create membrane pores to disrupt or lyse target cells?
defensins
when pseudopods completely wrap around a target cell, the vesicle that is
formed is called a what?
phagosome
when NK cells encounter a virus-infected or cancerous cell, they will respond by
releasing what?
perforins
what is produced by virus-infected cells to trigger
neighboring cells to produce antiviral proteins?
beta interferon
the classical pathway of complement activation requires what bound
to the target cell to bind C1 & start the cascade?
antibodies
complement fixation will trigger three protective effects: phagocytosis,
inflammation & the formation of the what?
membrane attack complex (C5-C9)
inflammation is commonly triggered by the release of what from Mast
cells or Basophils?
histamine
pyrogens are released by leukocytes, but mostly by what, to trigger fever?
macrophages
the automatic production of antibodies against A or B antigens of RBCs without
exposure to those antigens is called what?
innate immunity
vaccinations are administered to achieve what immunity?
induced acquired active
an antigen presented in a class I MHC will be recognized by a what cell?
cytotoxic T
antigen-presenting cells activate Helper T cells by displaying antigens in
glycoprotein receptors are called what?
class II major histocompatibility complex
what is the purpose of memory cells?
wait until next exposure & activate more quickly
activated Helper T cells function to secrete what?
cytokines
an activated B cell is called a what cell, and it functions to produce what?
plasma & antibodies
name the class of antibodies that are a monomer and are the most common in
your blood.
IgG
IgE antibodies function as a receptor on the surface of what cells &
basophils?
mast
the antigen-biding sites of an antibody adhere to the antigenic determinant site
or what of an antigen?
epitope
coating something with proteins like antibodies or C3b to enhance phagocytosis is called what?
opsonization
which lymphoid organ is expected to shrink with age?
thymus
lymphatic system functions
- reclaim lost fluid for return to cardiovascular system
- protect against pathogens & cancer cells
nonspecific defenses (lymphatic system function)
general protection, doesn’t distinguish threat specifics
specific defenses (lymphatic system function)
immune response, identify and defend against one particular threat
immunity
resistance to infection through activation of specific defenses
lymph (lymphatic system components)
fluid similar to plasma but less proteins
lymphatic vessels (lymphatic system components)
carry lymph from tissues to veins
lymphoid tissues & organs (lymphatic system components)
site of development of lymphocytes & screening for pathogens
lymphocytes & phagocytes (lymphatic system components)
provide defense
lymph & lymphatic vessels:
-lymph originates as fluid lost from blood capillaries
-collected in blind-end lymphatic capillaries
-overlapping endothelial cells
create one-way mini-valves
-fluid, solutes, large objects driven into lymphatic capillary by pressure in interstitial space (arteries, skeletal muscle)
lymphatic vessels:
-histologically most like veins
- all three tunics
- large ones have vasa vasorum
- many valves & anastomoses
- lymph nodes present along vessels
-converge, return fluid to bloodstream: lymphatic capillaries -> lymphatic collecting vessels -> lymphatic trunks -> subclavian veins
lymphangitis “blood poisoning”
inflammation of a lymphatic
vessel, due to toxins or infection, vasa vasorum swell with blood due to pressure appears as red line under skin
lymphoid cells
- macrophages
- dendritic cells
- lymphocytes -> 3 classes
-constantly circulates between blood, lymph, tissues & can survive for 20+ years
macrophages (lymphoid cells)
phagocytosis & T cell activation
dendritic cells (lymphoid cells)
antigen presentation (found in CT)
T cells (lymphocytes -> lymphoid cells)
-thymus-dependent
-80%
cytotoxic T/ Tc cells (T cells -> lymphocytes -> lymphoid cells)
kill “foreign” cells directly (cell-mediated immunity)
helper T/ Th cells (T cells -> lymphocytes -> lymphoid cells)
activate T & B cells
suppressor T/ Ts cells (T cells -> lymphocytes -> lymphoid cells)
inhibit T & B cells
B cells (lymphocytes -> lymphoid cells)
-“bone marrow-derived”
-10-15%
-when activated -> plasma cell -> secretes antibodies -> bind to specific antigens (foreign molecules)
-antibody-mediated or humoral immunity
natural killer/ NK cells (lymphocytes -> lymphoid cells)
-5-10%
-attack abnormal cells: cancer cells or virus-infected cells (nonspecific defense)
lymphopoiesis
production of lymphocytes
-occurs in bone marrow, thymus & lymphoid tissues
lymphopoiesis: hemocytoblast -> lymphoid stem cell:
-one type of lymphoid stem cell stays in bone marrow -> B & Nk cells
-one type migrates to thymus -> T cells
-both T & B cells divide to produce clones
-both migrate to all lymphoid tissues for division & development
lymphoid tissue
-reticular CT & lymphocytes & other lymphoid cells
-functions: proliferation & surveillance
-two types: lymphoid follicules & organs
functions of lymphoid tissues:
- proliferation site for lymphocytes
- surveillance point for lymphocytes & macrophages
lymphoid follicules/nodules (lymphoid tissue)
-CT packed with lymphocytes
-no capsule
-germinal center in middle: divides B cells
-germinal center surrounded by dendritic cells, T cells & macrophages
-follicles associated with respiratory, digestive & urinary tracts
MALT (mucosa-associated lymphoid tissue) (special lymphoid nodule/follicle collections)
deep to intestinal epithelium, made up of individual nodules called Peyer’s Patches
appendix (special lymphoid nodule/follicle collections)
tubular offshoot of beginning portion of large intestine
tonsils (special lymphoid nodule/follicle collections)
large nodules in pharynx, have crypts to trap bacteria -> encourage develop of immunity
- 5 total: 2 palatine, 1 pharyngeal (adenoid) & 2 lingual tonsils
lymphoid organs (lymphoid tissue)
-fibrous CT capsule around outside
-contain many lymphoid follicules
-include: lymph nodes, thymus & spleen
lymphoid nodes (lymphoid organs)
-bean shapes, 1-25 mm
-have associates blood vessels & nerves
lymphoid node structure:
-capsule: CT, surrounds outside
-trabeculae: folds of capsule creating partitions inside
-cortex: outer edge
-superficial cortex: lymphoid follicles (B cells & dendritic cells)
-deep cortex: T cells, transit between lymph & blood
-medulla: center, houses T, B & plasma cells
-sinuses
sinuses (lymph node structure)
spaces throughout house macrophages, allow lymph flow through node
lymph flow through node:
-lymph enters via afferent vessels
-flows slowly through sinuses where it surveys for pathogens & antigens
-macrophages engulf pathogens & dendritic cells bind antigens & stimulate lymphocytes
-“clean” lymph exits via efferent vessels
lymph nodes clustered mostly along lymphatic trunks:
function to purify lymph before returning it to blood
what happens when pathogens are detected in a lymph node?
-lymphocytes increase in number (rapid clonal division of B & T cells)
-causes buboes
buboes
lymph nodes swell
yersinia pestis
“bubonic plague”
-buboes all over body
lymphadenopathy
chronic enlargement of lymph nodes, due to infection or cancer
cancer often metastasizes in lymph vessels:
blood capillaries restrict access to cells but lymphatic capillaries don’t
thymus (lymphoid organ)
-glandular
-located superior to heart
-T cells mature in cortex & migrate to medulla to enter heart
thymus most active in early childhood, atrophies with age
thymosin & thymopoietin (hormones produced by thymus)
promote development & maturation of lymphocytes (mostly T cells in thymus)
functions of spleen:
-remove abnormal blood cells
-store iron from recycled RBCs for reuse
-initiate immune response by B & T cells in response to antigens in blood
-store platelets
-site of fetal erythrocyte production
red pulp (structure of spleen)
sinusoids filled with RBCs, platelets & macrophages which phagocytose old RBCs & pathogens
white pulp (structure of spleen)
lymphoid follicles containing lymphocytes, await antigen to activate
spleen cleans blood:
-blood flows slowly through sinusoids
-macrophages & lymphocytes detect & destroy foreign cells & antigens
spleen
-located lateral to stomach
-mostly sinusoids
-bleeds profusely when damages
-too fragile to stitch
-splenectomy to prevent fatal hemorrhaging
-liver & bone marrow can take over functions
defense against pathogens:
1st line: prevent entry -> skin & mucosa
2nd line: general antimicrobial actions when 1st line has been penetrated (innate defense)
3rd line: precision assault on a specific pathogen
physical barriers (nonspecific defense)
prevent approach if & deny access to pathogens
a. cutaneous membrane (skin)
b. mucosa
cutaneous membrane (skin) -> physical barrier -> nonspecifc defense
-impenetrable layers of keratinized cells
-impermeable to water & chemicals
-acid pH due to sebum
-high salt due to perspiration (acid & slat inhibit microbe growth)
mucosa -> physical barrier (nonspecific defense)
-produces antimicrobial secretions
-acids: inhibit microbe growth
-lysozyme: lyse bacterial cell walls
-mucus: traps microbes
microphages -> phagocytes (nonspecific defense)
-neutrophils & eosinophils
-either phagocytose pathogen
-secrete defensins on pathogen defensins cause membrane pores that cause lysis of target cell
macrophages -> phagocytes (nonspecific defense)
-phagocytose pathogens, cell debris & other foreign material
-remove debris & pathogens
-fixed & free macrophages
fixed macrophages (macrophages -> phagocytes -> nonspecific defense)
non-traveling, associated with specific tissue or organ ex: microglia
free macrophages (macrophages -> phagocytes -> nonspecific defense)
travel throughout body via blood
what do all phagocytes have in common?
-emigrate from capillaries
-display chemotaxis
-have receptors to bind targets for phagocytosis
phagocytosis 1-3
- microbe adheres to phagocyte via receptors on phagocyte
- phagocyte forms pseudopods that engulf particle
- phagocytic vesicle is fused with lysosome
phagocytosis 4-5
- microbe in fused vesicle is killed & digested by lysosomal enzymes within phagolysosome, leaving a residual body(undigestible)
-small solutes diffuse into cytoplasm for use - enzymes neutralized, indigestible & residual material is removed by exocytosis
immunological surveillance (nonspecific defense)
-monitoring of tissues by NK cells for abnormal cells (cancer or virus)
-abnormal cells express abnormal antigens on surface -> detected by NK cells
-NK cells bind abnormal cell & release perforins from Golgi
-perforins assemble on target membrane creating pores -> lysis of target
interferons (nonspecific defense)
-antiviral cytokines
-proteins released by activated lymphocytes, macrophages or virus-infected cells
-three types: alpha, beta & gamma
cytokines
chemical used for cell-to-cell communication
α interferons (interferons -> nonspecific defense)
produced by leukocytes to attract & stimulate NK cells
β interferons (interferons-> nonspecific defense)
produced by virus-infected cells to trigger neighboring cells to produce antiviral proteins to slow viral replication
γ interferons (interferons-> nonspecific defense)
produced by T & NK cells to stimulate macrophage activity
complement system
-attacks & breaks down cell walls, attracts phagocytes & stimulates inflammation
-antibacterial proteins
-11 complement proteins + 9 other factors & regulators act in cascade to cause foreign cell lysis (often target bacteria)
classical pathway (complement system -> nonspecific defense)
-requires bound antibodies
-C1 binds antibodies on bacteria
-turns on C2 + C4
-C3 converted to C3b
-C3b binds bacteria
alternate pathway (complement system -> nonspecific defense)
-no antibodies required
-factors P, B, D interact in response to foreign materials
-C3 converted to C3b
-C3b binds foreign material
complement fixation (complement system -> nonspecific defense)
-triggers anti-microbial effects
attachment of C3b, results in activation of antimicrobial effects: phagocytosis, inflammation & catalyzes formation of MAC
MAC
membrane attack complex
trigger phagocytosis -> complement fixation (complement system -> nonspecific defense)
attract phagocytes & makes bacteria easier to grab & digest (opsonization)
promotion of inflammation -> complement fixation (complement system -> nonspecific defense)
causes release of histamine from basophils & mast cells
catalyzes formation of MAC -> complement fixation (complement system -> nonspecific defense)
C5-C9 assemble to form pores on the membrane of the target cells resulting in cell lysis/death
inflammation (nonspecific defense)
localized redness, swelling, heat & pain in response to any tissue damage
functions of inflammation (nonspecific defense)
- help prevent injury/infection from spreading
- disposes of cell debris
- sets stage for repair
inflammation events 1 & 2 (nonspecific defense)
- histamine is released by mast cells in response to changes in local environment & triggers acceleration of blood flow to area (vasodilation)
- clotting factors & complement enter the site, a clot forms around injury & complement system lyses bacteria & attracts phagocytes
inflammation events 3 & 4 (nonspecific defense)
- local temperature rises due to increased blood flow, which acerbates enzymatic reactions to enhance killing of pathogens (causes redness & heat)
- neutrophils arrive, emigrate chemotaxis & activate to produce respiratory bursts, releasing toxic compounds to kill pathogens & release cytokines to attract other phagocytes
inflammation events 5 & 6 (nonspecific defense)
- macrophages arrive to engulf pathogens & cell debris
- fibroblasts are stimulated to create collagen patches (scar tissue) to reinforce the clot & begin repair
inflammation events 7 & 8 (nonspecific defense)
- mast cell chemicals trigger pain receptors
- the specific/immune defenses are activated
puss
dead WBC, pathogens, debris: failure to clear -> abscess
abscess
puss walled off by CT
necrosis
tissue degeneration due to lysosomal enzymes released by damaged cells (injury gets worse before better)
apoptosis
controlled cell death (no necrosis)
fever (nonspecific defense)
elevated body temperature (> 99°F/37.2 C)
-triggered by pyrogens, released into blood by leukocytes, mostly macrophages, upon exposure to foreign antigens
effects of fever (nonspecific defense)
increase metabolic rate to allow better defense & repair (rate increase 10%/1°C)
-up to 104°F: safe & productive
@106°F: nervous tissue dysfunctional
@110°F: proteins denature = death
T cell-specific or adaptive defenses (immune response)
cellular immunity, function to amplify the inflammatory response
B cell-specific or adaptative defenses (immune response)
humoral immunity responsible for most complement activation/fixation
specific or adaptive defenses = immune response
- B or T cell immunities
-each B/T cell covered in receptors that recognize & bond only one specific antigen
-simple chemical structures like plastic & metal aren’t immunogenic/antigenic
-responds to threats on a individual basis
antigen
foreign substance that can activate immune system & provoke a response
-usually large complex, molecules: proteins, nucleic acids, lipids, polysaccharides
forms of immunity
acquired, innate, acquired active, passive acquired, naturally acquired active, induced acquired active, induced acquired & natural acquired
antiserum
purified antibody solution against a particular antigen
acquired immunity (specific resistance immunity)
produced by prior exposure or antibody transfer
innate immunity (specific resistance immunity)
genetically determined, no prior exposure or antibody transfer involved
active acquired immunity (specific resistance immunity)
produced by antibodies that develop in response to antigens (immune response)
passive acquired immunity (specific resistance immunity)
produced by transfer of antibodies from another person
naturally acquired active immunity (specific resistance immunity)
develops after exposure to antigens in enviroment
induced acquired active immunity (specific resistance immunity)
develops after administration of antigens to prevent disease (vaccination)
induced acquired passive immunity (specific resistance immunity)
conferred by administration of antibodies to combat infection (antiserum)
natural acquired passive immunity (specific resistance immunity)
conferred by transfer of maternal antibodies across placenta or in breast milk
specificity (properties of immunity)
immune response targets particular antigens, each B & T cell responds to and destroys only one specific antigen
versatility (properties of immunity)
a large diversity of lymphocytes prescribed by genes exist to respond to almost any antigen, when a particular antigen is encountered, the one lymphocyte specific to it divides by clonal selection to produce many cells specific to particular antigen
memory (properties of immunity)
response after second exposure to the same antigen is faster, stronger & lasts longer, during the initial exposure memory cells were created to respond quickly upon second exposure
tolerance (properties of immunity)
immune system responds only to non-self antigens, B & T cells that recognize self-antigens are destroyed by clonal deletion to ensure self-tolerance
T cells & cell-mediated immunity
-targets virus or parasite-infected cells, cancer cells & cells of foreign grafts
-3 main types of cells: Tc, Th, Ts
-T cells must be activated by exposure to antigen
-doesn’t recognize free antigen
major histocompatibility complex (MHC)
antigen must be bound to special glycoprotein receptors on target cell
cytotoxic T (Tc) cells (T cell -> cell-mediated immunity)
carry out cell mediate immunity, physically attack foreign cells
helper T (Th) cells (T cell -> cell-mediated immunity)
activates B & Tc cells
suppressor T (Ts) cells (T cell -> cell-mediated immunity)
moderate the immune response by inhibiting Tc & B cells
class I MHC
-found on all nucleated cells: secreted by Golgi
*not in RBCs
-bind endogenous antigens: contain small peptides present in cytoplasm
-abnormal peptides (cancer, virus, bacterial) trigger cell destruction by Tc cells
class II MHC
-found on lymphocytes & antigen-presenting cells (ACP)
ex: macrophages
-bind exogenous antigens: material that has been phagocytosed & broken down
-activate Th cells which activate B cells & Tc cells
how is class detected/recognized by T cells?
determined by CD (cluster differentiation) markers on the T cell (glycoprotein receptors)
CD8 -> Tc & Ts:
responds to antigens in class MHC I
CD4-> Th:
responds to antigens in class MHC II
activation of CD8/Tc cells/Killer T
- cell finds target antigen in class MHC 1
- Tc cell undergoes clonal selection: proliferation producing many identical cells (stimulation from Th & activated by APC)
- some clones remain inactive as memory Tc cells
- some clones (active) destroy target cells: perforins, lymphotoxin & apoptosis
perforins & lymphotoxin
lyse target & disrupt DNA
graft rejection -> tissue typing
attempt to match MHC, but antigens in MHC will always be foreign thus attacked -> immune-suppressive drugs to suppress Tc cell activity to save graft
activation of CD4/Th cells
- bind antigen in class MHC II
- proliferation/ clonal selection
- memory cells
- activate Th cells
activated Th cells secrete cytokines that coordinate specific & nonspecific defense:
-stimulate production of memory T cells
-accelerate production of active Tc cells
-attract & stimulate macrophages & NK cells
-promote activation of B cells resulting in antibody production
B cell & antibody-mediated immunity
-targets bacteria, bacterial toxins & free viruses
activation of B cells: T-dependent antigens 1-3
- B cells have antibodies (IgD) on surface as receptors for antigens: binding causes B cells to become sensitized
- bound antigen is internalized & expressed back on surface in class MHC II
- specific Th cell recognizes antigen + MHC complex & releases cytokines to activate B cells
activation of B cells: T-dependent antigens 4-5
- activated B cell proliferates (clonal selection) to produce memory B cells & plasma cells
- plasma cells secrete antibodies specific to original antigen, ~2000/sec, for 4-5 days, then die (apoptosis)
some B cells respond to T-independent antigens:
-they can self-activate upon antigen binding without a Th cell
-T-independent activation is less common & produces much weaker response & less protection
initial exposure to antigen:
~5 days B cell -> plasma cell
~10 days to peak antibody levels (titer) in blood
-antibodies (IgM) circulate ~2 weeks
second exposure to antigen:
memory cell -> plasma cell ~1-2 days
-peak titer ~2-3 days, higher level
-antibodies (IgG) circulate week-months
antibody (Ab) structure
-two identical heavy chains (H)
-two identical light chains (L) all held together by disulfide bonds
-hinge region: flexibility
-humans produce 100 million-billion different Ab’s that each bind a different antigen
constant segments (C) (Ab structure)
-determine class of antibody molecule
-have sites for complement binding (Fc region)
fragment crystallizable region (Fc region)
the tail region of an antibody that interacts with cell surface receptors called Fc receptors and some proteins of the complement system
variable segments (V) (Ab structure)
-determine antigen specificity of antibody
-make up antigen binding sites (2 per monomer molecule)
IgG antibodies (class of antibodies/immunoglobulin)
-monomer (1Y)
-most common
-produced upon second exposure
-produced at high levels
-provides resistance against viruses, bacteria, toxins
-can cross placenta
IgM antibodies (class of antibodies/immunoglobulin)
-pentamer (5Y)
*10 binding sites
-first-class produced upon initial exposure
-forms immune complexes agglutination)
IgA antibodies (class of antibodies/immunoglobulin)
-dimer (2Y)
-in secretions (sweat, tears)
-surface protection
-inside/outside surfaces
*4 binding sites
IgD antibodies (class of antibodies/immunoglobulin)
-monomer (1Y)
-on surface of B cells as receptor
-sensitizes or activates B cells upon antigen binding
IgE antibodies (class of antibodies/immunoglobulin)
-monomer (1Y)
-on mast cells & basophils as receptor
-triggers histamine release upon antigen binding
antigen-antibody complexes
-antibodies bind antigens via antigen-binding sites
-antigen bound by its antigenic determinant site/epitope
complete antigen (antigen-antibody complexes)
two epitopes bound to the two antigen binding sites
incomplete antigen(antigen-antibody complexes)
only one epitope bound to one site (small molecules), can lead to allergies (combined with body proteins)
ex: latex
agglutination (effects of antibody binding)
enhances phagocytosis & reduces number of infectious units to be dealt with
opsonization (effects of antibody binding)
coating antigens with antibodies enhances phagocytosis
neutralization (effects of antibody binding)
a. blocks adhesion of bacteria & viruses to mucosa
b. blocks active site of toxin
complement fixation (effects of antibody binding)
activation of complement system
inflammation (effects of antibody binding)
-stimulate inflammation (IgE on mast cell)
-disruption of cells by complement/reactive protein attracts phagocytic & other defensive immune system cells
antibody-dependent cell-mediated cytotoxicity (effects of antibody binding)
antibodies attached to target cell cause destruction by non-specific immune system cells
*eosinophils
autoimmune disorders (immune disorder)
immune response targets normal body cells, autoantibodies produced
insulin-dependent diabetes mellitus/type 1 diabetes (autoimmune disorder)
attack cells of pancreas
multiple sclerosis (MS) (autoimmune disorder)
-attack white matter of CNS
-Tc cells
rheumatoid arthritis (RA) (autoimmune disorder)
-attack joints
-antibodies
graves disease (autoimmune disorder)
-stimulate thyroid
-overactivation/ overproduction of thyroxine
immunodeficiency disease (autoimmune disorder)
-immune system fails to develop or immune responses are blocked
-due to genetics /development, infection by virus, exposure to radiation or drugs
SCID (severe combines immune-deficiency disorder) (immunodeficiency disorder)
born without B or T cells
Hodgkins disease (immunodeficiency disorder)
lymph node cancer = decreased B & T cells
AIDS (acquired immune deficiency syndrome) (immunodeficiency disorder)
virus (HIV) infects CD4 (Th) cells & replicates causing cell lysis
-Th cells necessary for both Tc & B cell activation
-decreased Th -> patient has poor cell-mediated & antibody-mediated immunity
-patient dies of opportunistic infections
allergies
excessive immune response to non-harmful antigens results in tissue damage
immediate hypersensitivity (allergies)
-most common
-antibody-based
-antigen = allergen
a. anaphylaxis
b. atopy
anaphylaxis (immediate hypersensitivity)
-initial expose produces IgE
-IgE binds Mast cells/ basophils
-2nd exposure, allergen binds IgE, triggers release of histamine & heparin -> inflammation (ex: runny eyes & nose
anaphylactic shock
allergen circulates in blood -> body wide inflammation (decreased BP = shock)
atopy (immediate hypersensitivity)
full-blown allergic response upon 1st exposure
delayed hypersensitivity (allergies)
-cell-mediated
-Tc, Th & macrophages activated by allergen resulting in cell death & local inflammation (ex: poison ivy)
age-related changes
-thymus size decreases, fewer T cells produced
-decreased Th cells = less B & T cell activation = decreased immunity overall
- decreased B cells = decreased antibodies = increased susceptibility yo viral & bacterial infections
-increased chance of cancer (decreased NK & Tc cells)
