Immune system Flashcards
Why have an immune system?
- ubiquitous microbes
- the body has approximately 10 trillion cells, 1 trillion of these are dermal bacteria on our skin which we cannot wash off, and many intestinal bacteria
- many of these are harmless
- many are helpful (the microbiome for example)
- some are pathogenic (opportunistic - acquire the ability to cause a disease, ex: e-coli; most of them are benign but some can cause a lot of harm)
microbiome
ecosystem of bacteria in our intestinal tract
- has a huge impact on intestinal life and life long health
- birth canal in delivery
what are the good characteristics of having an immune system?
when the appropriate response is taken:
- can combat infection
- immune clearance (removing parasite or infection)
- tissue healing (to normal or almost normal)
- can prevent future infections
what are the bad characteristics of our immune system?
when an inappropriate response is made:
- the infection wins
- can be because of an overactive immune response (allergies - overactive response to something benign, in severe cases can cause extreme vasodilation, making blood pressure too low = death)
- or can be cause if immune system does not respond at all - immunodeficiency (when we get older this happens)
- can cause collateral damage (ex: getting a cut, becomes swollen, red, hot)
- system can be exploited by pathogens or parasites
which organ system is involved in our immune system
lymphatic system
which organs are involve din our immune system?
1) thymus - in chest, gets smaller as we get older (stops growing at puberty)
2) lymph nodes - scattered throughout the body where lymph moves through and where immune cells congregate
3) spleen - which we can live without, immune cell gathering place
4) bone marrow - source of all immune cells
5) appendix? - meeting point for cells, can live without
which two tissues are involved in our immune system?
1) MALT - mucosa associated lymphoid tissue
- this is not an organ, it is a tissue within an organ, part of the mucosa
2) GALT - gut associated lymphoid tissue
- where the immune system learns what’s outside the body
which two areas are said to be “immune privileged”?
1) the brain
2) the cornea
immune privileged refers to the fact that the immune system does not reach here
pathogen
“organism” that causes disease (we consider a virus a pathogen but it is not an organism
-patho = disease, gen = to create
immunogen
something that causes an immune response
-can be a whole organism or part of an organism
antigen
- always part of an organism, majority are proteins
- type of immunogen
- something that causes antibodies to be made - specific immune response (antigen and immunogen are used interchangeably)
antibody
molecule specific to an antigen
-molecule that we make that binds to a single antigen (to the epitope specifically)
epitope
one part of an antigen
- could be very small (15-25 AAs)
- this is the exact spot where the antibody binds
innate immunity is the ____ line of defence
1st
innate immunity
- 1st line of defence which is constantly active and exhibits a rapid response (almost immediate)
- a lot of the measures taken are preventative
- non-specific, antigen independent and reaches a broad range - ingests any bacteria, responds to all equally
- this system is not improved upon repeated exposure (no memory)
what 2 physical barriers are included in the innate immunity?
1) physical prevention - skin
- single layer epithelial cells in gut, prevents bacteria form coming in unless damaged
2) mucous membranes - keeps bacteria out
what are the 4 physiological barriers to infection
1) temperature
- increase in temperature makes environment less hospitable for bacteria - inflammatory reactions are warm
2) pH
- low pH of stomach, pH of sweat
3) enzymes
- in our tears and in mucus of nasal cavity, we secrete lysozyme - breaks down bacteria cell walls
4) compement
- proteins in our blood, prevents bacteria from reaching blood
what are the primary functions of complement
- lysis of foreign cells and bacteria (break down membrane and making them explode)
- a cascade of 30+ proteins
- pore (MAC) formation
MAC: a ring of proteins that forms a hole
-[] of solutes higher in cytoplasma than in ISF, without MAC, controls water rushing in
what are the secondary functions of complement?
- activation of inflammation
- opsonization of bacteria (covering them with something so they’re easier for immune cells to eat)
- immune clearance (getting rid of parasites)
what are the two ways in which complement can be “activated”?
1) having some of C1 proteins bind to foreign cell (recognize it) - this makes the pathway begin
2) can have a specific antigen on the cell surface, with an antibody which binds to pathogen and triggers the pathway (very specific)
regardless of mechanism, the end result is the same (MAC)
what does MAC stand for?
membrane attack complex, this is the end result of complement activation
what are the 4 granulocytes
1) basophils
2) mast cells
3) eosiniophils (stains blood)
4) neutrophils
which is the most common WBC?
neutrophils
what are the 5 phagocytes?
1) eosinophils
2) neutrophils
3) monocytes
4) macrophages
5) dendritic cells
what are the 5 antigen presenting cells?
1) monocytes
2) macrophages
3) dendritic cells
4) lymphocytes
5) plasma cells
name the lymphocytes
T cells, B cells, Plasma cells, and NK cells
I am a WBC that has lots of granule and many vesicles containing things such as enzymes, histamines, etc.
What am I ?
granulocytes
I am a WBC that ingests things and I am never found in the blood but you will find me in tissue
what am I ?
phagocytes
I am a WBC that helps the acquired immune system see pathogens/parasites
Who am I?
antigen presenting cell
neutrophils
- 50-70% of WBCs
- polymorphonuclear cells (another word for neutrophil)
- irregularly shaped nucleus, between 3-5 lobes
- short lived, highly effective phagocytes (1 or 2 days)
- early recruits during infection
eosinophils
- 1-3% of WBC
- most hang out near epithelia - see them in gut and lungs, these are areas we tend to get infected with larger parasites
- defence against large parasite
- phagocytotic cells - forms pocket on parasite and kills it
basophils and mast cells
- rare
- these are non-phagocytic - do not ingest anything
- release compounds such as histamine or chemotaxins
- histamine causes vasodilation, more blood = more neutrophils to infection site
- chemotaxins are attractive molecule - neutrophils or other WBCs detect it and move towards it
what are the two ways in which a cell can die
1) apoptosis
2) necrosis
apoptosis
- programmed cell death
- all content of the cell remain in little compartments after the cell dies, this makes it easier to clean up by other cells (who eat them)
- energy is required
necrosis
- cell death
- cell swells and pops - the severity of the disease is greater when cells die from necrosis
- no energy required to die this way
- pneumonia is an example of necrosis, all the stuff that was inside the cell goes into body once it explodes
macrophages
- these come from monocytes (which are 1-6% of WBCs)
- residential cells
- very long lived - up to months, keep tissue clean
dendritic cells
residential cells
-long membrane processes
_____ immunity is not a specific response whereas ____ immunity is very specific
innate, acquired
what are PAMPs?
pathogen associated molecular patterns
-these allow us to recognize which cells are foreign so we don’t kill our own cells
what are the 4 PAMPs?
1) Gram+ bacteria - make peptidoglycan
2) Gram- bacteria - make lipopolysaccharides (LPS)
3) fungi - make zymosan (yeast cell)
4) viruses - make dsDNA, ssRNA
these associated compouds are then recognized by TLRs, activating their associated macrophage
Toll-like receptors (TLRs)
a class of proteins that play a key role in the innate immune system. They are single, membrane-spanning, non-catalytic receptors usually expressed on sentinel cells such as macrophages and dendritic cells, that recognize structurally conserved molecules derived from microbes
- these activate their associated macrophage
- PAMPs activate these
which has a second outer membrane? Gram+ or Gram-?
gram -, gram+ has a thicker cell wall
briefly explain bacterial reocognition
PAMPs bind to TLRs on macrophages or mast cells which activates them, leading to phagocytosis
phagocytosis
- ingesting a foreign particle - into a phagosome (body/compartment within the cell)
- there is a lisosome inside the cell that contains enzymes that can break down/damage DNA
- vessicles fuse together (phagolysosome) and kill bacteria by O2-independent mechanisms or O2 dependent mechanisms
- degraded material can be used by the cell, or dumped out and removed by kidneys - presented to T cells
phagocytosis: O2 independent mechanisms
- a way of killing bacteria that does not require O2
- lysosome and other hydrolytic enzymes (breaks down pepsidoglycan)
phagocytosis: O2 dependent mechanisms
- a way of killing bacteria that is O2 dependent
- reactive species - cells consume O2 and convert it inro molecules, bacteria gets chopped up into pieces
O2 dependent killing
- reactive oxygen species (ROS)
- reactive nitrogen species (RNS)
- respiratory burst - rapid increase in oxygen consumption
- oxygen is converted into super-oxide, creating hypochlorous acid
- can make reactive nitrogen species as well
-this can make very dangerous substances (ex: peroxynitrie)
lymphocytes mainly play a role in acquired immunity, but what is the one INNATE lymphocyte?
the natural killer (NK) cell
explain the death by NK cell
- these are innate lymphocytes (the only ones)
- they kill altered self cells (virus infected, cancerous)
- examine every cell they see to see if it’s healthy
- if a cell gives a positive signal AND a negative signal, it is not killed
- if a cell ONLY gives a positive signal, it will be targeted by the NK cell
when talking about death by NK cells, why don’t unhealthy cells give off a negative signal?
- unhealthy cells release interferon alpha - which stops the negative signal
- PERFORIN punches a hole in the cell membrane and GRANZYME B goes through the opening and induces apoptosis
chemotaxins - def
molecules that attract phagocytes to a site of infection
cytokines - def
proteins released by one cell that affect the growth or activity of another
opsonins - def
proteins that coat pathogens so that phagocytes recognize and ingest them
antibodies - def
proteins secreted by B cells that fight specific invaders
complement - def
plasma and cell membrane proteins that act as opsonins, cytolitic agents, and mediators of inflammation
C-reactive protein - def
opsonin that activates the complement cascade
granzymes - def
cytotoxic enzymes that initiate apoptosis
histamine - def
vasodilator and bronchioconstrictor released by mast cells
interferons (IFN) - def
cytokines that inhibit viral replication and modulate the immune response
interleukins - def
cytokines secreted by leukocytes to act primarily on other leukocytes; IL-1 mediates inflammatory response and induces fever
lysozyme - def
an extracellular enzyme that attacks bacteria
perforin - def
a membrane pore protein that allows granzymes to enter the cell; made by NK and cytotoxic cells
what are the cardinal signs of inflammation
1) rubor (redness)
2) tumor (swelling)
3) calor (heat)
4) dolor (pain)
5) functio laesa (loss of function)
step 1 in inflammation: chemical signals
-bacteria releases chemical signals that are detected by PAMPs - recognized as being foreign
second step in inflammation: mast cells
- one of the first cells that detect chemical signals
- release HISTAMINE - mast cells degranulate which causes vasodilation
- endothelial selectins - membrane bound molecule that allows a WBC to grab onto it, neutrophils have molecules on their surface that can bind selectin
- chemotaxins are released which attract neutrophils, highest [] of these are near site of infection
step three in inflammation: neutrophils
- extravasation - process of neutrophils getting out of blood vessel
- margination: moving from center where the blood flow is fastest to the end of the vessel
- rolling: slowing down and eventually stopping
- arrest: stopping after rolling
- diapedesis: migrating through the spaces between endothelial cells
fig 24.12
step 4 of inflammation: phagocytosis by neutrophils
- once neutrophils are in the tissue
- when enough have come in and eat bacteria
step 5 in inflammation: neutrophil elimination
- once all the bacteria have been eaten by neutrophils, need to get rid of neutrophils
- apoptosis and necrosis - necrosis would be a big problem
step 6 in inflammation: macrophages
- these are what induce phagocytosis on neutrophils
- clean up the mess, through resident macrophages (each tissue has these)
inflammation is a local response
true or false?
true (usually)
what causes redness in inflammation?
vasodilation
what causes swelling in inflammation?
fluid build up in the area - by neutrophils crossing the endothelium, this is why we feel pain
what causes heat in inflammation?
comes from neutrophils eating and killing all bacteria - increase in oxygen consumption and in chemical reactions, every reaction produces heat
what is pneumonia?
a lung inflammation
- the body’s normal response
- neutrophils infiltration, the neutrophils that were called in to get rid of bacteria don’t get filtered out
- very low gas exchange capable
- neutrophils get engulfed by phagocytosis
- increased chance that cells die by necrosis and cause enzyme release, destroying tissue
what is the second line of defence?
acquired immunity
- naive cells that require ‘education’
- need to learn what makes an appropriate response
- this immunity has a memory and is highly specific (antigen dependent)
what are the lymphocytes of acquired immunity?
Th cells
Tc cells
B cells
Plasma cells
what does each cell of the acquired immune system do?
1) Th cells direct
2) Tc cells kill
3) B cells differentiate into plasma cells
4) plasma cells generate antibodies
which region of the B cell receptor makes it unique?
the Fab region, which is where antigen binding happens
what is the Fc region of the B cell receptor?
where the antibody is one of 5 types
-IgA, IgG, IgM, IgD, IgE
the B cell receptor (BCR) - def
a unique surface antibody (immunoglobulin) molecule (IgM or IgD)
-these recognize one single antigen
how are B cell receptors made?
- they are made at random, by gene segment rearrangement
- the light chains are made up of a random sequence of VDJ (51 V, 27 D, 6J)
- heavy chain is made up of one random selection from either u (IgM), sigma (IgD), omega (IgE), gamma (IgG), of alpha (IgA)
fig 24.9
which is the most common antigen?
IgG
which antigen is found in breast milk?
IgA
what is clonal selection
- one antibody responds to a single antigen (lock and key)
- this then initiates clonal selection (activates)
- activation leads to division (proliferation) - expansion of the same cell (clonal expansion)
- differentiation - plasma (effector) cells produce 2000 antibodies per second - memory cells are created
during clonal selection of B cells, which can change? the Fc region or the Fab region?
Fc, but not Fab
clonal selection for primary immune response
- this is when an antigen is encountered for the first time
- clonal selection happens, proliferation, differentiation
- the end result is:
- memory cells (not involved in response)
- plasma cells (from B cells)
- this antibody production takes a long time
- about 7-14 days - response does not start until day 7
fig 24.8
clonal selection for secondary immune response
- when an antigen is presented for the second time (or third, or fourth, etc.)
- memory cells
- this leads to a rapid response (within 1-2 days) and a greater response
- memory for one antigen does not help for memory of another
- do not experience symptoms from the bacteria in this case
what are the 5 functions of antibodies?
1) antigen clumping/inactivation
2) lead to phagocytosis
3) lead to cell lysis
4) B cell activation
5) Mast cell degranulation
antibody functions: antigen clumping/inactivation
- in most instances, the antibody binds first to the antigen, forming the antibody-antigen complex. (immune complex)
- each antibody molecule can bind to two different antigen particles, one on each arm
- this creates clumping of antigens, which facilitates their recognition and destruction by the immune system
-in some cases, instead of binding to antigens, antibodies inactivate toxins produced by the bacteria
antigen clumping increases the rate of ______
phagocytosis
how can antibodies act as opsonins?
- includes the Fc region of the antibody-antigen complex
- activating Fc receptors on neutrophils and macrophages initiates phagocytosis - antibodies act as opsonins
what happens when the Fc region of the antibody is activated on basophils, mast cells, NK cells, or eosinophils?
- triggers degranulation, the release of chemicals stored in the immune cell
- receptor binding opens Ca++ channels, and Ca++ entry is the signal for exocytosis
the Fc receptor found on mast cells are specific for the Fc region of the _____ antibody family. What happens when these bind?
IgE, when IgE antibody-antigen complexes bind to mast cell Fc receptors, the cells degranulate releasing chemicals that mediate the inflammatory response
is complement the result of Fab activation or Fc activation of the antibody?
Fc region
what are the non Fc mediated actions of antibodies?
-activates B lymphocytes (B cells) - these then differentiate into plasma cells that secrete more antibodies
T lymphocyte development
- T cells are produced in the Bone marrow by stem cells (T cell precursors) and migrate to the thymus to become ‘specialized’
- T cell precursors both have CD8 and CD4 on them, a T cell that loses CD8 becomes CD8+ (cytotoxic cell) and one that loses CD4 becomes CD4+ (helper cell)
cototoxic T cells (CD8+) bind to MHC____ and helper T cells (CD4+) bind to MHC____
I, II
T cell receptors (TCR) are specific for every antigen
true or false?
true
T lymphocyte (T cell) specificity
- done by gene segment rearrangement
- TCR exists in 3-4 segments - up to 109 different variations which leads to over 22 million combinations
- high site of mutation as well
what does TCR recognize?
- antigen presentation - but these cannot recognize antigens without help, need to be shown the antigen
- major histocompatability (MHC) receptors
MHC class I
- nearly all nucleated cells
- these present ENDOGENOUS antigens (created inside the cell, many of them are self antigens, cancer)
- cytotoxic (CD8+) cell TCR are the only ones who recognize these
MHC class II
- antigen presenting cells
- activates macrophages, dentritic cells, and B cells
- helper (CD4+) cell TCRs are the only ones who recognize these
- present EXOGENOUS antigens (made outside the cell, internalized by phagocytosis) - some can be self antigens, some can be foreign
acquired immune specificity of EXOGENOUS antigens
- MHC class II molecules
- found primarily on antigen presenting cells (APC): macrophages, B cells, dendritic cells
- when an immune cells engulfs and digests an antigen, the fragments are returned to the immune cell membrane combines with MHC-II proteins
- if a helper T cell encounters an APC with a foreign antigen fragment on its MHC-II (as a whole complex), the Th cell responds by secreting cytokines that enhance immune response (2 positive signals activate the T cell)
fig 24.13
acquired immune specificity for ENDOGENOUS antigens
- MHC class I molecules
- found on all nucleated human cells
- when viruses or bacteria invade the cell, they are digested into peptide fragments (by proteosomes) and loaded onto MHC-I platforms (8-10 AA segment on MHC-I)
- if a cytotoxic (CD8+) T cell encounters a human host cell with a foreign antigen fragment on its MHC-I, the Tc cell recognizes the host cell as a pathogen infected cell and kills it (apoptosis) to prevent reproduction
clonal selection of T cells
- harder to measure than B cells
- TCRs from naive T cells that come from the thymus recognize a single Ag-MHC complex
- once their shown their antigen-MHC complex, they begin to divide
1) Effector T cells
- effector Th - produce cytokines (start giving orders which direct specific immune response; endocrine, paracrine, autocrine)
- effector Tc - cells kill the target - direct the specific immune response
2) memory T cells
- circulate until next encounter
what are superantigens?
- really strong antigens, they confuse your immune system by activating a large number of T cells
- when T cells look at MHC it’s not specific for, it binds anyway and holds it together (“awkward long hand shake”)
- this leads to polyclonal activation (up to 5% of Th cells are activated)
- systemic activation (mass cytokine release)
some diseases caused by this are staphylococcal enterotoxins and toxic shock syndrome
properties of cytokines
- they bind to specific receptors and once they are bound:
- signal transduction
- gene activation
- response
- different cytokines lead to different responses
- cascade induction (not only lymphocytes produce cytokines)
- one common cascade induction:
- IFN-gamma activates macrophages - which produce interleukin-12 which activates Th cells - positive feedback, helps T cells release more cytokines, making the system more robust
what are the 5 functions of cytokines?
1) autocrine, paracrine, or endocrine function
2) pleiotropy - one cytokine can have multiple effects on multiple targets
3) redundancy - many cytokines have the same effect on many cell types
4) synergy - if we release IL-4 and IL-5 for example, effects on C cell will be greater than the sum of each individually
5) antagonism - two different cytokines will have opposite effect on the same target (ex: IL-4 activated, IL-gamma shuts down B cells)
why do Th cells drive the immune response?
they are the main source of cytokines (production and/or release)
IL-4 _____ B cells while IL-gamma _____ B cells
activates, shuts down
what are the two major cytokine families?
Th1 cytokines and Th2 cytokines
Th1 cytokines
- IFN-gamma (stimulates macrophages and cytotoxic T cells - cell mediated immune response - T cells are activating other cells to kill ad remove pathogen; done by macrophages and cytotoxic T cells)
- IL-2
- GM-CSF
- IL-3
Th2 cytokines
- IL-4 (humoral responses, stimulate B cells which create antibodies, no cells are involved, ONLY antibodies)
- IL-3
- IL-5
- IL-10
what is the cause of tuberculosis?
- myobacterium tuberculosis
- 3 million deaths/year
- 1.8 billion current infections
- aerosolized bacteria - sneezing, coughing, get infected by inhaling
- alveolar macrophages ingest tuberculosis which prevents phagolysosome formation
- macrophage lysis (explode) and this causes tissue damage
what is the effective response for tuberculosis?
- leads to activation of Th1 cells
- release of IFN-gamma activated macrophages - ingest more bacteria, can override bacteria’s defense mechanism and force fusion/formation of phagolysosome
- cell mediated
- more alveolar macrophages - IL-12 activated Th1 cells
- further activated macrophages (positive feedback) some are still being lysed and damaging tissue
-so a wall forms around the bacteria - called granuloma (bacteria cannot escape anymore because this gets calcified)
how do vaccinations work?
- induce immune memory because secondary immune response is much faster
- natural immunity - to an encountered pathogen
- vaccines mimic the pathogen but it is attenuated (cannot cause disease) or purified (isolate proteins on molecule and inject those)
- these cause a slow primary response so that a subsequent exposure will be wuick
considering the millions of different BCRs and TCRs, and their all made randomly, why don’t we react to our self cells?
- we can, autoimmune diseases
- antigen recognition leads to an immune response
- multiple sclerosis - mylein basic protein
- insulin dependent diabetes - beta cell antigen stops producing insulin
- systemic lupus erythematosis - snRNPs
- but most are unknown
what is self tolerance?
- refers to the non-self reactive cells that escape
- dendritic cell - MHC receptor
- if a self antigen binds to the MHC, and causes a long interaction, the cell is terminated, if there is a short interaction, cell is allowed to live
what is the simplest form of life?
viruses
-they are not living organisms, they cannot reproduce on their own - they need a host cell
virus - def
infectious particles made up of nucleic acid (DNA or RNA) and protein
- surrounded by a membrane (capsid)
- they need host cell machinery for their own reproduction
viruses exist in two phases, what are they?
1) extracellular - virion
2) intracellular
what is the first phase of a virus? explain it
- extracellular - virion
- metabolically inert - there is nothing going on inside them, they are transmission forms to get from one cell to another
what is the second phase of a virus? explain it
- intracellular phase
- once it is inside the host, reproduction using the host’s machinery
- viruses exist as replicating nucleic acids (using ribosomes to make proteins_
what are the two viral binding proteins?
- hemagglutinin (HA)
- neuraminidase (NA)
what facilitates entry of viruses into cells?
- virions have viral binding proteins (antigens) that can bind to the host cell which leads to internalization of nucleic acids
- if we can block it, we can prevent entry
humoral immunity is highly effective at clearing virion, how does it do this?
- aggulination - clumping organisms or viruses together (with antibodies)
- in this case, there are fewer inefective particles, this also enhances phagocytosis (HA and NA are less able to get into cell)
virion clearance: antibody blocking
- anti-Ha and anti-Na
- entire surface of virion is covered, anti-HA binds HA and vice versa
- if the virus is coated with antibodies, H and N cannot reach the cell membrane, virus cannot get in - this is also a form of opsonization, inducing phagocytosis
virion clearance: activation of complement
- protein cascade that poke holes into membrane
- complement removes the envelope of the virion, proteins are embedded in this envelope, so the remaining virus (RNA or DNA) cannot enter cell because it no longer has the means to bind to it
- innate immune system
antibodies are ineffective against the intracellular stages of a virus, so how do we clear it?
- cell mediated immunity - the cell has to be targeted
- the self cell has now been ‘altered’ due to virus
- cytotoxic (CD8+) T cells are presented viral antigens
- NK cells (innate immunity) react to the cells in which the inhibitory signal has been removed (interferon alpha)
Leishmaniasis
- leismania and macrophages
- enters the phagolysosome, allows fusion, but enzymatically destroys reactive oxygen species faster than they can be created
what are the appropriate immune responses to leismaniasis?
Th1 response: leads to protection - produces interferon gamma (activates more macrophages) which increases ROS to overcome parasite
-CELL MEDIATED IMMUNITY
Th2 response: this response is INEFFECTIVE - susceptible to all symptoms of the pathogen, releases interleukin-4 which activates humoral B cells
-HUMORAL IMMUNITY
which response is necessary in order to control leishmaniasis?
Th1 response leads to protection, Th2 is useless
what happens in leishmaniasis if a Th1 mouse is given a IFN-gamma blocker?
-inhibits Th1 cytokine production, this leads to basically the same reaction a Th2 mouse would have, severety of disease much higher
what happens when we give a Th2 mouse anti-IL-4?
-this inhibits the Th2 cytokine production, the initial state of disease is about the same but decreases much more than in a Th2 mouse
females tend to be Th1 dominant, so how does this affect pregnancy?
- developing an embryo is like a foreign object, the Th1 response would attack it
- so females switch to Th2 during pregnancy, leads to remission of Th1 mediated diseases
-pregnant Th1 mice respond more like Th2 mice
African sleeping sickness
- chronic fatigue
- trypanosoma spp. (single cell parasite of blood)
- blood borne infection
- progresses to a neurological CNS disease
a humoral (Th2) response is effective - because this parasite is extracellular
- variant surface glycoprotein (VSG) - molecule that trypan. has on membrane
- the majority (99%) of the parasites are eliminated (complement, opsonization, phagocytosis) - by mounting an immune response to VSG
however…. VSG is constantly changing so immune cells don’t know what they are anymore (primary response is always going on, slow)
VSG1 response kills 99% (primary immune response), remaining 1% has to be killed by VSG2 response (another primary response)
-cycle keeps going, no secondary responses
