JG Day 2- Immunity and Infection Flashcards
What is the gram stain classifications?
- Gram +
- Gram-
- other (acid fast, nothing)
What are the shapes of bacteria?
- Cocci- spherical
- Bacillus- rods
- other- spiral
How do the oxygen requirements vary among bacteria?
- Aerobic- exposed to air (skin, resp tract)
- microaerobic- lil o2 needed (stomach)
- facultative anaerobic- anaerobes that can use O2 if available
- obligate anaerobic- O2 is toxic to them, live places deep in body
What is toxin formation by bacteria?
- Toxins produced by bacteria to kill other microbes
- endotoxin- from gram - bacteria, release by bacterial cell death i.e. LPS)
- Exotoxin - come from gram + bacteria, secreted from live bacteria, i.e. botulinum toxin)
- or no toxin produced
these toxins are not intended to harm us. most abx are toxins from microbes but they are not toxic to us
What is the spore formation by bacteria?
- Spores are formed by bacteria when bacteria is in danger (think like an escape pod)
- spores are VERY hard to get rid of
Are bacteria extra or intracellular?
Most are extracellular
intracellular bacteria are harder to get rid of
What is staphylococcus?
- Gram positive
- Cocci
- Aerobic
- in clusters
What is streptococcus?
- Gram positive
- cocci
- aerobic
- in chains/pairs
What is clostridium?
- Gram positive
- Rods
- Anaerobic
- spore forming
What is bacillus?
- Gram positive
- bacilli
- aerobic
- spore forming
first bacteria named- bacillis antracis which causes anthrax
What is listera?
- Gram positive
- Bacilli
- aerobic
- non-spore forming
Surgeon that discovered listera discovered that if you clean instruments between patients, patient outcomes are better
What is bacteroides?
- Gram negative
- rod
- anaerobic
most common cell in body
What is neisseria?
- Gram negative
- SPheres
- Pairs
Causes gonnorhea
What determines gram staining?
- Gram positive bacterium has a thick peptidoglycan layer
- gram negative bacterium has a thick peptidoglycan layer and an outer membrane
- this prevents the staining (usually purple violet) from entering peptidoglycan layer
gram staining dermines whether or not bacteria has outer wall
What is bacteria DNA like?
- one, single, circular, double stranded chromosome
- contains all genes that bacteria needs to code for whatever it needs to do
What are plasmids?
- Code for 1-6 genes
- carry a “superpower” for the cell
- the bacteria is able to share this superpower with other cells
- this is how we produce insulin.
- give DNA for producing insulin to bacteria. Bacteria share the plasmid by combining with other bacteria via a pillus
- then we harvest all the insulin made and kill the bacteria
- also make other peptide drugs via this method
What are viruses?
- True parasites
- needs to get INTO cell to do anything
- all intracellular
- needs to get INTO cell to do anything
- virion binds to cell, gains entrance.
- only gets into cell with that cell speicfic protein
- species and cell speicfic
- only gets into cell with that cell speicfic protein
- DNA of virus puts gene in our DNA and then replicates
- new viruses then use our plasma membrane and go off to another cell
What are 2 interesting methods where we can utilize viruses?
- gene therapy- can give cell a virus with copy of good gene, then virus will replicate good gene (i.e. for sickle cell to replicate good hemoglobin)
- if virus has protein that’s useful, we keep it
- 2% of genes come from viruses
What are the medically relevant fungi?
- Candida albicans
- normal gut flora
- cuases opportunistic infections- when you’re already not feeling good, yeast makes you feel worse”
- Aspergillis
- highly aerobic
- respiratory infection
- Tinea- not a speicifc fungus but gneeral term for skin fungus
- tinea cpitis- head
- tinea cruris- groin (jock itch)
- tinea pedia- feet (athelt’s foot)
What are megakaryocytes?
- pieces bud off to become platelets
- not immune cell
3 families of WBC?
- Mononuclea pagocytic system
- Polymorphonuclear leukocytes
- lymphocytes
What is a mononuclear phagocytic system?
- monocytes- when they leave blood they become macrophages
- macrophages- named based on where they are located
- kuppfer cell- liver
- microglia- brain
- dust cell-lungs
- osteoclast-bone. not immune cells but a lot of macrophages together to eat the bone
-
multinuclear giant cell- kind of like osteoclasts but are immune cells
- if fighting off big infection, amcrophages aren’t big enough to handle it. a bunch of macrophages will then get together and form multinuclear giant cells
- Dendritic cell (NOT macrophages)
- langerhans cell-skin
What polymorphonuclear leukocytes?
- Neutrophil- most plentiful
- Basophil
- Eosinophil
- Mast cell
sausage shped nuclei which can squeeze through endothelial cells to get from blood to tissue
What are the 3 types of lymphocytes?
- B-cells
- T-cells
- NK- natural killer cells
Types of B cells?
Plasma cells
memory cells
Types of T-cells?
- Tc- cytotoxic T cells- CD8
- Th1-helper 2 cells- CD4
- TH2- helper T cells CD4
- Memory cells
Order of frequency of immune cells?
- Neutrophil
- Lymphocytes
- monocytes
- eosinophils
- basophils
“Never let monkeys eat bannas”
Which immune cells are in tissue, not blood?
macrophages, dendritic cell, mast cells
What is humoral vs cell-mediated immune system?
- Humoral= fluid, in blood (Extracellular)
- Cell-mediated= intracellular
What is innate vs adaptive immunity?
- innate- born with it, always on
- adaptive- learns, but only happens when exposed. slower response time
Which immune cells are humoral?
- Innate: Myeloid cells- non-host epitopes
- Adaptive: B-cells- antibodies (also Th cells, APCs)
Which immune cells are cell-mediate?
- Innate: NK cells
- MHC existence
- Goes around asking cells if they’re virally infected. If infected, NK cells tell cell to kill themselves.
- however, viruses can hijack cell and tell cell to shut up
- Adaptive: Tc-Cell
- MC1-TCR
- will hunt you down and kill the cells if virally infected
- MC1-TCR
How do cells of innate immunity work?
- Macrophages all over body, waiting for something to happen
- detects bacteria from a skin cut (for example)
- signals release of cytokines/chmokines- magic fairy dust that tell imune cells to leave blood and go to tissue
- detects bacteria from a skin cut (for example)
- Cytokines and chemokines cause endothelial cell retraction to allow neutrophils to leave
- also allow plasma protein to leave, losing oncotic pressure, causing fluid to leave and cause edema
- Inflammatory cells migrate into tissue releasing infllammatory mediators that cause pain
- also cause swelling around injured site.
What is the function of macrophages?
- Phagocytosis and actiation of bactericidal mechanisms
- antigen presentation
Function of dendritic cells?
- Antigen uptake in peripheral sites
- antigen presentation in lymph nodes
What is function of neutrophil?
- Phagocytosis and activation of bactericidal mechanisms
What is funciton of eosinophil?
killing of antibody-caoted parasites
What is function of mast cell?
release of granules containign histamine and other active agents
What is order of inflammatory reactions?
- Edema (from endothelial retraction)
- neutrophils- clean up damage
- macrophages- repair damage
- one lonely macrophage to begin with. this macrophage signals that injury has occured via cytokine/chemokine
- thousands neutrophils come
- then more macrophages join after in order to repair the tissue
What is the process of phagocytosis?
- Diffusion of chemotactic factors from site of injury
- adhesion molecules on endothelial cells and neutrophiles (pavementing)
- retraction of endothelial cells (Vascular permeability)
- movmeent of neutrophils through opened intercellular junctions into tissue
- neutrophils move up cytokine concentration gradient (crawl) to get to injury location
- neutrophils then pagocytose whatever they can
- will initial look for non-host epitose
- produce H2O2 (hydrogen peroxide) and dumps it into vesicle with bacteria to destory bacteria
What is a PAMP?
- Pathogen associated molecular pattern. What antibodies look for to bind to
Are phagocyte looking for bacteria?
No, looking for a antibody stuck to something
What is role of B cells?
- Adaptive immunity
- B cells from bone marrow and make antibodies
- antibodies made from plasma cells (transformed b cells)
What are Tcells?
- Come from thymus
- Adaptive immune system
- 2 types
- cytotoxic- investigate host cells to see if it has a virus and then kill host cells with virus
- helper t cells
- help b cells mature and function
What is the process of making B/T cells?
- Lymphoid stem cell released form bone marrow
- goes to thymus to become immunocompetent, naive T cell or bone marrow to become immunocompetent, naive B cell
- Then migrate to secondary lymhoid organs (i.e. lymph node, tonsil, spleen) to find antigen
- once activated by antigen, B cells mature to plasma cells and produce antibodies
- T cells are activated by antigen exposure and then become Th cells or cytotoxic tcells and do their function
What are central lymphoid tissue?
primary
- thymus
- bone marrow
What are peripheral lymphoid tissues?
- aka secondary
- adenoid
- tonsils
- lymph nodes
- spleen
- peyer’s patches (ileum only)
*
Which 2 organs do not have lymph nodes?
Brain
Kidney
What is an epitope?
Some molecular pattern we can grab onto
(found on antigens)
What is an antibody?
- binds to antigen
- y-shaped
- “hands” of Y are binding unit to epitope (location on antigen we bind to)
- antigen-specific
- has 2 light chain, 2 heavy chain
- consists of areas of heavy chain and parts of light chain that are constant
- part of light chain is variable, where antigen binding sites are
What are the diff types of immunoglobulins?
- IgM- first immunoglobulin then differentiates into other classes
- IgA- secreted into GI tract
- IgE- antibody of peripheral tissue
- IgG- antibody of blood
- (Ignore IgD for this class)
What is the Fab?
binding site of antibody (part that is variable for each antibody)
How do antibodies protect the organism?
- bind to:
- toxins- toxin then neutralized
- bacteria- phagocytes now more aggresively eating bacteria
- virus- virus is then unable to bind to receptor on host cell and is ineffective
antibodies make immune system more effective but we don’t want antibodies to bind to us!
How are B cells made?
- A single progenitor cell (from bone marrow) gives rise to a large number of lymphocytes, each with a different genetic specificity on the variable portion (making different locks)
- Nurse cells present varying proteins (from out body) to the made B cells to see if any self-react
- If any B-cells self react, those B cells are destroyed (called clonal deletion)
- We now have a pool of mature lymphocytes that may, or may not work against any antigen BUT we know they aren’t self-reactive
- If the b-cell created finds it’s antigen, then we know this is a useful B-cell and we should make more and more antibodies (immunoglobulins) are produced by mature, activated B-cell (clonal selection)
What is the immune reaction to a parastitic worm?
- Parasitic worm dead in interstitial space (this parasite has antigens)
- B-cell comes along and the parastiic worm antigen matches to it
- starts replicating and converts to plasma cell to start secreting antibodies
- antibody binds the mast cell and if the parastie antigen binds to the antigen, then the mast cell will degranulate and release ECF-A (eosinophil chemotactic factor of anaphylaxis)
- this goes to the vasculature and promots endothelium retraction to allow eosinophils to get through vasculature
- eosinophils attach parasite. attack enhanced once antibodies bind to parasite’s surface
What is the difference between a primary and secondary immune response?
- In primary immune response, IgM is the first antibody to respond
- IgG then peaks later (because of class switch from IgM to IgG)
- On the second exposure (secodary immune response), we have memory cells, so IgG peaks first and rises very quickly. IgM has same response as before
What is the secretory immune system?
- IgA sit underneath mucosal lining in organs exposed to “outside” aka mucosal-associated lymphoid tissue (airways, esophagus, GI tract) so antigens can be found quickly
What is a peyer’s patch?
- Gut Associated Lymphoid Tissue
- M cell takes things form lumen of GI tract (in ileum) and move it underneath, so any antigen will be transported under basal lamina so it can be exposed to B/T cells.
- The B cells convert to IgA (with the help of helper T cells) and then gets secreted back into lumen of intestine
What is the placental syncytiotrophoblast?
Cells forming placenta join together and form one large plasma membrane, which stop substances from getting through gap junctions in cells
- we actually acquired this from a virus
How are maternal IgG’s transported to the fetal circulation?
- Fc receptors located on maternal circulation side that recognize the IgG antibody
- The IgG antibody is then endocytosed and is protected from lysosomal digestion durign transport fo the vacuole across the cell (aka transcytosis)
- on the fetal side of the syncytiotrophoblast, IgG is released by exocytosis
What are the antibody levels in umbilical cord and neonatal circulation?
- Maternal IgG is shared with the fetus and will almost reach adult levels by birth.
- After birth, maternal IgG levels quickly fall and child’s IgG begins to increase
How do T cells work?
- T cell still makes binding site in a similar method as b cell (randomly arranging DNA)
- however, a t-cell always has the binding site attached to the cell, it is never free floating (unlike b-cell and their antibodies)
- t-cell only has one binding site
- t-cell isn’t actively looking for an antigen, but has antigens presented to itself by an MHC (major histocompatibility complex)
- In order to t-cell immunity to funciton, need same TCR, MHC and antigen in order to bind
What are the 2 classes of MHC?
Class I and Class II
What is class I MHC?
- Has 3 subclass- HLA-A, HLA-B, HLA-C
- reacts with CD8 on Tc (cytotoxic) cells
What are class II MHC?
- 3 different genes- HLA-DR, HLA-DP, HLA-DQ
- Reacts with CD4 on Th (helper) cells
How do class I MHC work?
- Cell chops up protein that we just made and presents it as an antigen on an MHC
- That MHC is transferred to the surface and presented at the cell surface
- if a T-cell comes along and binds, then we know the antigen is foreign (because we got rid of all our self-reacting t-cells)
- therefore, we know the cell is virally infected
- therefore, the cell needs to die
How does a class II MHC work?
- Cell phagocytoses a substance, chops it up and then presents the antigen at the cell surface
- if a t-cell responds to the antigen, then that means the antigen is foreign
- we want this cell to continue phagocytosing and killing other bacteria/foreign substances
What are APCs?
- professional Antigen Presenting Cells
- only 3 cells present MHC-II to helper cells
- dendritic cells
- macrophages
- b-lymphocyte
What cells express class I MHCs?
every cell in the body that has a nucleus (RBC do not have nuclei)
How are t-cells developed in the thymus?
- Lymphoid stem cell comes into thymus, is differentiated into T-cell
- T-cell is presented to self-antigens in same process as b-cells
- ones that react to self are destroyed (this is called negative selection)
- The t-cells then go on to be presented to MHC
- t-cells that bind to MHCs are made (positive selection)
What are immune privileged sites?
- Placenta/fetus
- testes and ovaries
- eyes
- brain
- thymus
How do lymph nodes drain lymph?
afferent–> lymph node–> efferent lymphatic vessel
Why do lymph nodes swell during infection?
- Lymph nodes have b/t cells waiting to find antigen
- once they find an antigen, they replicate
- copious amount of b cells replicating causes swelling of lymph nodes
- lymph node nearest to infection will be most swollen
What is dendritic cell role in capturing antigens?
- immature dendritic cell will pick up antigen in tissue, e.g. skin and migrate to lymph node
- dendritic cell become mature after picking up antigen
- Naïve helper T-cell in lymph node interacts with mature dendritic, will find its antigen and signal reactions
- Activation of a B-cell by a T-cell independent antigen
We usually need T-helper cell to activate B-cell but with presentation of a repetitive antigen can activate B cell without it
What is hypersensitivity disorder?
Response of immune system is out of proportion to the effect
- Four diff types: I, II, III, IV
- I, II, III are antibody mediated
- IV- t-cells
What is Type I hypersensitivity?
- Immune Reactant- IgE (in peripheral tissue)
- Antigen- soluble antigen
- effector mechanism- mast-cell activation (granulation)
- example of hypersensitivity reaction- allergic rhinitis, asthma, systemic anaphylaxis
Ex- allergy to cat dander in house.
Very fast activation
What is Type II hypersensitivity?
- Immune reactant- blood
- Antigen- cell or matrix associated antigen
- Effector mechanism- FcR cells (phagocytes, NK cells)
- Example of hypersensitivity reacion- some drug allergies (i.e. peniccillin). Blood transfusion reaction, hemolytic disease of newborn, graves’ disease, myasthenia gravis
IgG binding to our own ECF protein
- immune system assumes that if antibody binds, then it’s foreign and needs to be destroyed
What is Type III hypersensitivity?
- Immune reactant- IgG
- Antigen- Soluble antigen
- Effector mechanism- FcR cells complement
- form immune complex of antibody and antigen.
- hyperreaction and clumping up blood vessels
- get stuck to wall
- then neutrophils, macrophages come to attack the antigens stuck to the blood vessel wall
- now causing blood vessel damage
- example- serum sickness, arthus reaction, lupus, necrotizing vasculities
Way too much antigen and IgG causing immune complexes to get stuck on blood vessel and damaging blood vessel in process
What is Type IV hypersensitivity?
- Immune reactant- T cells
- soluble antigen or cell-associated antigen
- examples- transplant rejection, hasimoto’s thyroiditis, type 1 diabetes, poison ivy
Standard transplant rejection, CD8 cells looking for foreign cells and neutrophils going to attack (also poison ivy)
What is the soruce of antigen for Type I hypersensitivities?
environmental antigens
What is autoimmunity?
self-antigens
What is alloimmunity?
immune response to another “person’s” antigens (ie pregnancy)
What are some examples of Type I allergy hypersensitivities?
allergic rhinitis
anaphylaxis
asthma
What are some examples of type II hypersensitivities with environmental allergies as a source?
hemolysis with penicillin (didn’t talk about in class…)
(RARE)
What is an example of type III environmental allergy hypersensitivity?
wheat gluten
also rare.
What is example of type IV hypersensitivity caused by environmental allergen?
poison ivy
What is an example of type II autoimmunity hypersensitivity?
graves disease
myasthenia gravis
(2/3 all autoimmune are type II)
What is an example of Type III autoimmunity hypersenesitivity?
Lupus
necrotizing vasculitis
What is an example of type IV autoimmunity?
Hasimoto’s thyroiditis
type I diabetes
What is example of type II alloimmunity hypersensitivity?
bad blood transfusion
hemolytic dx of newborn
hyperacute graft rejection- happens intraop. incredibly rare
What is example of Type III alloimmunity?
serum sickness
Example of type IV alloimmunity hypersensitivity?
transplant rejection
What is the mechanism of a type I, IgE mediated reaction?
- First exposure to an allergen stimulates B lymphocytes to mature into plasma cells and produce IgE
- IgE is absorbed to surface of mast cell by binding with IgE specific Fc receptors
- when adequate of IgE is bound, causes mast cell sensitization
- During 2nd exposure, allergen cross-links surface boudn IgE and causes degranulation of mast cell
- Initial phase has
- vasodilation
- vascular leakage
- smooth muscle spasm
- glandular secretions within 5-30 min
- Late phase occurs 2-8 hours later
- results from infiltration of tissue with inflammatory cells
What are some manifestations of a type I hypersensitivity reaction?
- Itching
- Angioedema
- edema of larynx
- urticaria
- bronchospasm
- hypotension
- dysrhythmia
- GI cramping
What is mechanism for Type II hypersensitivity reactions?
- Antibody (IgG) binds to antigens on cell surface and destroys or prevents cell from functioning by
- complement mediated lysis (erythrocyte can be target)
- phagocytosis by macrophages in tissue
- neutrophil mediated destruction
- antibody dependent cell mediated cytotoxicity
- modulation or blocking the normal function of receptors
- Ex-
- Myasthenia gravis- Antibody binds to ACh receptor and blocks ACh from working
- leads to progressive weakness/paralysis
- Graves’ disease- antibody binds to TSH
*
- Myasthenia gravis- Antibody binds to ACh receptor and blocks ACh from working
What does O blood contain (antigen and anibodies)
Blood O group have core H antigenic carbohydrates
Have A and B antibody in serum
What does A blood contain? (antigen and antibody)
A blood has H antigenic carb modified into A antigens
Antibody against B antigen
What does type B blood contain (antigen and antibody)
Type B blood has core H antigen modified to B antigens
Blood also has antibody against A antigen
What does type AB contain?
Antigen has A and B
No antibodies in blood
What is mechanism for Type III hypersensitivity?
- Immune complex disease
- relatively uncommon- lupus and overadministration of albumin are examples
- aggregates stick to side of vessel, end up damaging BL
- big problem in lupus is kidneys
What is mechanism for Type IV hypersensitivity?
- T-cell is self reactive
- helper T-cell- upregulate immune system out of proportion
- cytotoxic t-cell- will go around killing everything
- Usually auroimmune dx and transplant
- with transplants- we match MHC (HLA)
What is the pathogenesis of autoimmunity?
- Arises from many common
- inheritance of susceptibility genes that may interfere with self-tolerance
- generally MHC linked
- environmental triggers (inflammation, other inflammatory stimuli) that promote lymphocyte entry into tissues, activation of self-reactive lymphocytes and tissue injury
- inheritance of susceptibility genes that may interfere with self-tolerance
- becoming more prominent and virulent
- typically some trigger causes the self reactive cell to become activated
- cell responds appropriately, and fights infection but then turns to own cells
Examples of rheumatic autoimmune ddiseases?
Rheumatoid arthritis
Scleroderma
Sjogren’s Syndrome
Lupus
What are some GI autoimmune diseases?
Chronic active hepatitis
Crohn’s disease
Primary biliary cirrhosis
Ulverative colities
What is an example of endocrine autoimmune diseases?
Graves’ disease
Hashimoto’s thyroiditis
Type 1 DM
What are some examples of neurologic autoimmune diseases
multiple sclerosis
myasthenia gravis
Examples of hematologic autoimmune diseases?
Autoimmune hemolytic anemia
idiopathic thrombocytopenic purpura
pernicious anemia
Examples of renal autoimmune diseases
goodpasture’s syndrome
Mutli organ autoimmune diseases?
Ankylosing spondylitis
polymyositis
psoriasis
sarcoidosis
vasculitis
What is systemic lupus erythematosus?
- Inherited susceptibility genes
- class II MHC
- Complement
- other
- Environmental triggers
- UV irradiation
- Both susceptibility and environmental triggers and cause cellular necrosis, dumping intracellular contents into plasma
- nuclear proteins become antigens to system (B-cells not exposed to the nuclear proteins since they should be intracellular)
- Activation of helper T cells and B cells
- IgG autoantibody production
- Immune complex and autoantibody-mediated tissue injury
Who tends to be more affected by autoimmune disease? When do they tend to be intiated?
Women more affected than men
Mainly occurs during times of hormonal fluctuation
What are 2 types of immune deficiency?
- Primary (genetic)
- lymphoid
- SCID- both B and T cell affected
- ADA deficiency
- txmt- bone marrow transplant
- Agammaglobulinemia- only B cell affected
- Di George syndrome- T cell affected
- SCID- both B and T cell affected
- myeloid
- chronic granulomatous disease
- lymphoid
- Secondary (acquired)
- HIV
Where’s the normal location for B and T cells in lymph nodes?
Outer cortex= b cells
Inner cortex= t cells
What are some immune problems with phagocytes?
- Leukocyte adhesion deficiencies- won’t be able to stop neutrophils that are rolling along inside blood vessels
- Chornic granulomatous disease- lack catalase so can’t make H2O2 to kill pathogen
- myeloid problem
What is HIV?
- Cell speicfic for T-helper cells (CD4)
- Binds to helper cells, injects RNA
- RNA–> DNA with reverse transcriptase
- DNA inserted into our DNA
- We make it’s mRNA
- it’s mRNA used by our ribosomes to make protein
- big protein is then cut up into little pieces
- virus then uses our plasma membrane to go on to other cells
What are some treatments for HIV?
- Entrance inhibitors- prevent virus from entering cells. not very popular
- Reverse transcriptase inhibitors- prevents RNA–> DNA process. We don’t do reverse transcriptase in any other cell of body
- Integrase inhibitors- prevent Proviral DNA from being impelemented into out DNA
- Protease inhibitors- prevent the viral protein from being chopped up and sent off to other clels
What is the conversion of HIV–> AIDS?
- T helper cells present antigen on MHC I- presenting foreign protein and cytotoxic cell kills the Thelper cell
- Measure of HIV progression is T helper cell count
- <400 = AIDS
What is mycobacterium?
- Tuberculosis- acid fast staining
- intracellular (often macrophages)
- waxy coating- leads to cseous necrosis in TB
- Types:
- m tuberculosis: TB
- M. leprae: leprosy
- M. avium- intracellular- TB like dx in immunodifienct pt
- starting to come back where HIV rates are high
- US TB rates are decreasing
- Worldwide- tb rates are increasing
From picture:
- Host response in absent T cell-mediated immunity. In both cases (pic shows example of myco. avium and M. leprae), no granulomatous response; intracellular bacteria persist and proliferate within macrophages, because there are inadequate T cells (in case of AIDS) or T cells don’t appropriately activate macrophages to kill intracellular pathogens (lepromatous leprosy)
What is toxic shock syndrome?
superantigen induce inflammatory response
- superantigen- (ie bacterial toxins) bind directly to TCR and MHC II molecules
- superantigens activate Th cells independently of TCR antigen specificity
- Superantigen binds very tightly and indiscriminately to TCR and MHC II
- T cell activates helper cells and get SUPER activated
- ramps up immunes system to crazy levels and causes anaphylaxis shock
- causitive agent-
- streptococcus pyogenes
- staphylococcus aureus
- streptococcus pyogenes
How does HIV affect CD4 cells?
- Decreased lymphokine produciton
- loss of stiumuls for T and B cell activation
leads to:
- lymphopenia
- decreased CD4/CD8 cell ratio
- decreased delayed hypersensitivity
makes you more susceptible to opportunistic infections
How does HIV affect CD8 cell?
- Impaired cytotoxic activity
- impaired feedback
How does HIV affect macrophages?
- Decreased chemotaxis and phagocytosis
- diminished IL-1 production
- impaired presentation of antigen to T cells
How does HIV affect B cells?
- Diminished antibody production in response to antigen
- production of immunoglobin
Causes non sepcific increased serum immunoglobin
