Lymphatic / Immune notes

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Contents

[edit] Lymphatic system

  • Only responsible for what is in class today.
  • There are vessels and tissues / organs.
  • Vessels do two things:
    • Carry interstitial fluid back to the circulation system
    • Absorb fat from the intestines and carry lipids and lipid soluble vitamins back to the circulation (ADEK).
    • Carry stuff through the lymphoid tissues.
  • Lymphoid tissues and organs
    • site of maturation of phagocytic cells and T and B cells.

[edit] Vessels

  • 3 liters / day are leaked out of capillaries.
  • This contains fluids and proteins.
  • Note that the composition doesn't change, we just change the name.
  • Also note that unlike blood vessels, lymphatic vessels have "blind ends".
  • The endothelial cells that line the lymphatic vessels are not joined tightly and thus proteins and fluids can get into the vessel. They are however, linked such that fluids do not easily flow outward, from vessel to interstitial cells.
  • The cells around the vessel will move apart as the vessel fills such that the fluid, proteins, and microorganisms can continue their easy flow.
  • There are one way valves to discourage backflow.

[edit] Movement of lymph

  • It is slow, propelled mostly by muscle movement (that is skeletal muscle movement). Thus, people who stand for a long time tend to have swelling in their lower extremities.
  • Elephantitis occurs because of a parasitic infection that blocks the lymphatic system from returning fluid to the circulation system.

[edit] Lymphoid cells, tissues, and organs

  • Lymph nodes found throughout the body.
  • B and T lymphocytes and macrophages make up the cells.
  • Tissues are the diffuse tissues found all over the body, not just part of the drainage system.
  • Organs:
    • Primary: produce lymphocytes.
      • red bone marrow and thymus
    • Secondary: where the lymphocytes mature
      • lymph nodes, nodules, and the spleen.

[edit] Thymus

  • Different than other lymphoid tissues because it is not very reticular.
  • It has two lobes.
  • This is where the T cells mature and they learn to distinguish self from non-self.
    • This process starts very early in development but becomes less important until the thymus atrophies.
  • Blood-thymus barrier protects T cells from antigens.

[edit] Lymph nodes

  • Vessels come in (afferent), send fluid through the many compartments such that microorganisms interact with T lymphocytes, macrophages, and B lymphocytes in order to allow for immune reaction.

[edit] Spleen

  • Found on left side of the stomach.
  • It removes lots of RBCs and platelets.
  • The spleen can store platelets.
  • It can also generate RBCs (usually in the fetus, animals, and under great duress).
  • The spleen is not necessary in adults.
  • The spleen is amorphous and hard to fix, so we remove it when injured; bone marrow and liver can take over function.
  • Largest of the lymphoid organs.
  • Removes material from blood.

[edit] Diffuse tissue

  • Tonsils:
    • recognize and remove things that are foreign from nasal and oral cavities.
  • Peyer's patches:
    • in the small intestine and respiratory system.
    • similar to tonsils.
    • Function to recognize and remove pathogens.
    • Prevent bacteria from entering the intestine.
    • Similar to spleen.

[edit] Immunity

[edit] Innate defenses

  • These are things like defensins and compelement.
  • We'll just consider this anything that is non-specific.

[edit] Physical barriers

  • Skin
    • Has acidic secretions.
  • Gut
    • Gastric secretions are acidic, too.
  • Mucus
    • Of respiratory tract.
    • Traps pathogens, gets ejected (blow your nose!).
  • Tears and saliva
    • Have bacteriacydal traits (contain lysosyme).

[edit] Phagocytes

  • Monocytes differentiate into macrophages.
  • Phagocytes include monocytes, eosinophil, free macrophages, neutrophils, and fixed macrophages.
  • Kupffer, alveolar macrophages, and microglia are macrophages in the liver, lungs, and neuro tissues.
  • How do they work?
    • They respond and move toward chemotaxants which might be given off by pathogens or by other immune or phagocytic cells.
    • They adhere to the target cell with their microvilli.
      • The microorganism may be coated with complement, too, which would help with latching on.
    • Then they engulf it.
    • Then fuse their lysosomes and granules with the microorganism's vesicle.
  • TB pathogens live in phagocytic vesicle demonstrating that this method doesn't always work.
  • When the phagocyte gets done, it releases the material including enzymes which can cause inflammation and pain.
  • Cool pictures of this.

[edit] Natural killer cells

  • NK cells recognize body cell that have been infected with viruses or have turned cancers.
  • NK cells recognize a spectrum of epitopes, not just one.
  • Don't engulf but kill by releasing chemicals that cause lysis of abnormal cell.
  • NK cells move to the cell, form an adhesion to the target cell.
  • This stimulates the movement of the golgi to the junction of the cells.
  • Then the golgi starts pumping out porferin.
  • Then vesicles full of porferin will fuse to the NK membrane thus dumping them very near the membrane of the target.
  • Then porferins form a pore in the target cell and allow for the flow of stuff such that the cell dies.

[edit] Interferons

  • These are glycoproteins released by lymphocytes and macrophages usually in response to viral infection. Virus infected cells can also release these interferons.
  • They come as alpha, beta, and gamma; mostly alpha and beta.
  • Alpha is produced by leukocytes and attract NK cells.
  • Beta is produced by fibroblasts and slows inflammation.
  • Gamma is produce by NK cells and T lymphocytes and induces macrophages to recognize infected cells and helps stimulate antibody-antigen response.
  • They have been cloned and are clinically available.
  • But they are not magic bullets because they gear up the whole immune system such that any propensity for autoimmune reactions generate lots of side effects.
  • Alpha Interferons are affective for some viral infections like AIDS, herpes, and hepatitis.

[edit] Fever

  • The warmer it gets the less pathogens can proliferate.
  • Protentiates the effects of interferons.

[edit] Inflammatory responses

  • Mast cells (and others) can generate inflammatory responses.
  • This causes pain, swelling, increased blood flow, activation of phagocytosis, increased capillary permeability, activation of complement system, increase of clotting near region of infection, increase of temperature in the infected area, and activation of specific defenses.
  • Picture of mast cell releasing granules containing histamine.
  • read the articles.
  • stopped here on 01/27/10.
  • started here on 02/01/10.
[edit] Article: Mast cells show their might
  • Mast cells are key to the interface between the innate immune system and the adaptive immune system.
  • Mice that don't have mast cells cannot fight infections well.
  • Why not?
    • Mast cells contain toll-like receptors that recognize bacterial proteins.
    • When bacteria lands on these receptors, mast cells release TNF because of activation of some intracellular pathways.
  • TNF then causes the mobilization of neutrophils.
  • TNF also causes lymph nodes to release lymphocytes.
  • So, if you don't have mast cells, you still have a reaction, but it ins't sufficient to beat the infection.
  • Mast cells also cause some problems, however:
    • Allergies.
    • Initiation of rheumatoid arthritis may be due to mast cell release of IL1.
    • Though we don't know much about it, mast cells may also have activity in MS, heart disease (mast cells release stuff that might encourage formation of plaque), and tumor growth (via inflammation and also angiogenesis).
[edit] Goals of inlammation
  • Temporary repair of the area.
  • Slowing spread or killing pathogens.
  • Mobilize local, regional and systemic defenses in order to kill pathogens and regenerate damaged tissue.
  • Remember that heparin is an anticoagulant.
  • Histamine and heparin attract phagocytes, first the neutrophils, then the macrophages.
  • Phagocyte mobilization is achieved by chemotactic signals given off by microbes, prostaglandins, and other neutrophils.
    • Neutrophils within minutes, 8-12 hours later come macrophages.
  • Different phagocytes are recruited with different time courses.
  • Low doses of aspirins inhibit prostaglandins.
[edit] Article: Internal affairs
  • Question of the paper: Can the non-specific immune systme recognize and react against micro-organisms already inside the cell?
  • Answer: yes
    • There is a surveillance system that parallels the one detecting microorganisms outside the cell.
  • The cellular resonse varies from instigating inflammation to apoptosis.
  • Cells appear to have internal receptors that recognize motifs on micro-organisms (like toll-receptors).
  • There may also be many othe receptors that recognize other abnormal compounds like urate and asbestos (very different molecules), etc. The intracellular receptors are not as well characterized as the external ones.
  • They describe the inflammasome as a complex of proteins. It causes the secretion of inflammatory encouraging enzymes.
  • The inflammasome activates Caspase1 which activates ILs.
  • The ILs lead to an inflammatory response.

[edit] Interface between the specific and non-specific

[edit] Complement

  • We call this an interface because it is important in both systems.
  • Name describes it as something that complements the function of antibodies.
  • This system involves multiple proteins in a cascade mechanism.
  • These proteins are found in the blood as inactive components.
  • Proteins C1-C9, though there are sometimes more than one protein with a number designation.
  • There are also separate proteins that are regulatory and cofactors: B, D, and P.
    • These proteins for an alternative pathway to the cascade.
  • The classical pathway:
    • Includes C1-C9.
    • Initiated by antibodies that are bound to their target.
    • C1 then attaches to the antibodies.
    • Then C1 is activated and it cleaves C3 with C2 and C4 as cofactors.
    • Finally, C3b is bound to the surface of the target cell (not to the antibodies).
  • The alternate pathway:
    • Sugars on the surface of pathogens initiate the process.
    • Sugars allow for C3 to cleave on its own.
    • Then C3b ends up on the cell surface.
  • The presence of C3b on the surface of the target causes:
    • attraction of phagocytes through chemotaxants (called opsonization),
    • stimulation of phagocytosis,
    • stimulation of inflammation.
    • activation of C5-C9,
      • C3b cleavage of C5 into C5a and C5b)
      • C5b and other C proteins form the membrane attack complex (MAC),
      • This allows free flow of crap in and out and kills the cell.
  • C3a and C5a are proteolytic byproducts which cause mast cell degranulation which leads to histamine release and inflammation. So all this is very integrated and concerted.
[edit] Functions of the complement system
  • Lyse cells by poking holes.
  • Increase capillary permeability by stimulating histamine release through mast cells through C3a and C5a.
  • Coat the surface of microbe with signals for phagocytosis via opsonization via C3b.
  • Secrete chemotactic signals to recruit phagocytes.

[edit] Innate immunity

[edit] Innate versus acquired immunity

  • The innate immune system is the first responder by recognizing a broad range of antigens and we are born ready to do this.
    • Found in invertebrates and "lower life forms".
  • Acquired immunity is a reaction against a specific with a specific response and must be developed over time.
    • Found only in vertebrates.

[edit] Pathogens have distinct molecular patterns that are recognized by the innate immune system

  • PAMPs!
  • Examples: lipopolysaccharides (LPS) of gram negative bacteria, glycolipids of mycobacteria, mannans (long chain carbs) of yeast, or the dsRNA of viruses.

[edit] Innate immunity

  • Contains NK cells, macrophages, complement, and defensins.

[edit] Article: Innate immunity: ancient system gets new resepct

  • Defensins are a potent anti-microbial peptides that work by permeabilizing the membrane.
  • Defensins found throughout the animal kingdom.
  • When a particular Toll receptor binds it's ligind causes the synthesis of specific defensins.
  • We don't know how defensins are specific to pathogens and not host cells.
  • Zasloff did first work.

[edit] Versatile defensins

  • Defensins may have other activities, too.
    • Suggestions that it may be part of the acquired immune system:
      • Research in the aids field has shown that there are factors secreted by T lymphocytes which inhibit HIV from infecting cells.
    • Defensins are secreted by leukocytes as chemotractants for APC for the acquired immune system.

[edit] Innate versus adaptive immune system

  • Why have both?

[edit] Innate immunity is fast, acquired is slow

  • They aren't different systems, they are interacting systems that work together.
  • It is the cytokines from the innate that gears up the specific immune system.

[edit] "Innate immunity communicates its biological evaluation of an antigen to the acquired immunity"

  • It does this by:
    • secreting cytokines by macrophages and NK cells,
    • attachment of complement protein to antigens,
    • preferential uptake of antigens by leptin receptors antigen presenting cells.

[edit] Acquired immune system

[edit] Specificity

  • An antigen is something that is recognized by specific immune system as foreign.
    • These are usually over 10 kda.
    • Sugars and lipids are not very antigenic, but when added to a protein, they can become antigenic.
  • A hapten:
    • A small molecular weight compound that can become antigenic when complexed with another substance.
    • An example is poison ivy, which is a small, lipid toxin (hence crossing the skin barrier) that becomes antigenic when combined with a protein in the body.
  • An epitope (antigenic determinant) is a 3D part of the antigen that is recognized by the receptor / antibody.
    • These can be as small as 9 aas.
    • The recognition of these epitopes is preprogrammed in the immune system.
    • A given B lymphocyte will only make antibody A, that is, a protein that can bind a particular epitope.
    • You're born with all the B cells you will ever have.

[edit] Versatility

  • The human immune system can recognize 10^9 epitopes.
  • But there are only 10^5 genes, so how do we get all these? "What's up here?"
    • We get them all through genetic recombination.

[edit] Memory

  • After you've been exposed once, your response will be stronger and faster than before.

[edit] Tolerance

  • Means that the specific immune response does not react to the antigens of the host cells.
  • MHC = HLA (human leukocyte associated antigens).
    • These are glycoproteins on the cell surface.
[edit] MHC proteins
  • Type I MHC:
    • Found in all nucleated cells in the body.
    • These are unique proteins that work to define "self".
    • These are responsible for causing organ rejection.
    • One needs a match of about 75% of the MHC proteins in order to have a successful transplant.
      • This is a little misleading because some are more important than others.
  • Type II MHC:
    • Found only on cells in the immune system and determine the antigen presenting cells.

[edit] Systemic

  • The reaction is not confined to a local tissue.
  • The reaction will reach the entire body.

[edit] Cells of the acquired immune system

  • T cells
  • B cells generate antibodies for targeting for phagocytosis.
  • You must have a phagocytic cell that can present the antigen to the lymphocytes.
    • So, we consider macrophages as part of the specific immune system as well as the innate.
  • You are born with all your B and T cells that can be used, then you activate them throughout life.
    • Many will never be activated.
  • B and T cells come from the bone marrow and the lymphoid stem cells.
  • Lymphoid stem cells that go into they thymus and thus generate T cells.
    • In the thymus, they are selected against too-strong reaction to host antigens.
  • Lymphoid stem cells can also mature in the bone marrow to generate B cells and NK cells.

[edit] Antibody mediated immunity

  • Humoral immunity = antibody mediated.
  • B cells produce antibodies.
  • Antibodies can temporarily inactivate some organisms. 
Why only temp?
  • Abs target organisms for destruction by phagocytes or complement.
  • Abs are effective against dissolved antigens in the blood and extracellular pathogens (they can't get inside host cells).

[edit] Cell-mediated immunity

  • T cells work best against intracellular pathogens like fungi, viruses, cancer cells, and foreign tissue transplants.
    • This is because APCs present antigens to tell the T cell that a certain cell is infected.
    • Note that it is the T lymphocytes that attack transplanted tissue.

[edit] Antigen recognition and response to antigens

  • B lymphocytes can recognize soluble circulating antigens.

[edit] Cytokines

  • Both B and T cells are potentiated by cytokines including interferons and interleukins.
  • So we thought we could just administer these things to gear up the immune system to get rid of cancers and such.

[edit] Types of T cells

  • Cytotoxic T cells eat bad guys.
  • T helper cells, when activated, stimulate T and B cells by secreting cytokines.
  • Suppressor T cells inhibit the responses of T and B cells by secreting soluble mediators which inhibit the immune response.
    • These mature slowly and proliferate late to allow for a reaction and then start shutting it down.

[edit] Antigen presentation

  • T cells cannot recognize antigens by themselves.
  • The T cell must bind the antigen with other proteins found on macrophages and B cell surfaces.
  • Pathway for presentation:
    • via macrophage:
      • macrophage eats some pathogen.
      • macrphage breaks down the pathogen and it's proteins.
      • binding of antigen and MHC protein stabilizes the complex and causes it to be expressed on the cell surface,
    • via intracellularly infected cell:
      • cell breaks down pathogen proteins,
      • MHC binds antigen and gets expressed on cell membrane,
    • along comes a T cell and if it binds both its antigen and CD8 (which indicates that the cell with this antigen is a host cell),
    • This causes the T cells to proliferate....
  • stopped here on 02/01/10.
  • started here on 02/03/10.
  • In an infected cell, the microbe is broken down and the proteins are attached to a type I MHC and presented on the membrane.
    • Now T cells recognize the antigen and the host cell's MHC class I via CD8.
    • Some T cells turn into memory cells. Most become active, though.

[edit] The two types of MHC proteins are recognized by two tpyes of receptors on T cells

  • CD8 proteins recognize MHC class I. It is found on cytotoxic T cells.
  • CD4 proteins recognize MHC class II. It is found on helper T cells.
  • MHC I is presented on any nucleated cell.
  • CD8 T cells can become cytotoxic t cells, memorty Tc cells, and suppressor T cells.
  • CD4 T cells can become hleper T cells and memory Th cells.
    • Helper cells help make this process go by release of cytotoxins.

[edit] Cytotoxic T cells

  • CD8 T cells kill by
    • disruption of cell metabolism via lymphotoxins,
    • they stimulate apoptosis via cytokines and
    • they destroy the cell membrane via porpherins.
  • If the cell that presents is a macrophage:
    • Then CD4 cells bind to them because that's who bind CD4 cells.
    • This allows for release of cytokines.
    • The cytokines:
      • stimulate non-specific defenses and macrophages,
      • attract NK cells,
      • promote B lymphocyte proliferation and maturation and thus antibody production,
      • stimulate T cell proliferation and stimulation.

[edit] Importance of helper T cells

  • AIDS destroys CD4 cells.
  • AIDS recognizes and destroys CD4 protein and enters cell.
  • So as CD4 cells decrease from 1k to 200 / ml, infections increase.
  • Death occurs due to infections and cancers.
  • So, yes, helper T cells are required.

[edit] Suppressor T cells

  • Also called regulatory T cells.
  • Develop more slowly than other cells so there is a lag in their activity.
  • They help turn off the response.
  • They regulate the immune response.
  • They are the least understood of the T lymphocytes.

[edit] Fetal immune system hushes attacks on maternal cells

  • Maternal cells don't react to the fetal cells and vice versa.
  • But the fetus does respond to other exogenous cells.
  • This paper suggests that there isn't an immune response because T reg cells are upregulated.
    • This remains to be proven.

[edit] Can worms tame the immune system?

  • Indicates two important factors:
    • Complexitiy of the immune system,
    • Unintended side effects of treatment with drugs.
  • A doctor treated kids for parasitic worms. Then they became more sensitive to allergens.
  • This indicated that worms may dampen the immune system.
  • This has been confirmed with other experiments, but sometimes the worm is worse than the antigen.
  • So we did some research in mice:
    • Infected them with worms, showed that allergic responses were decreased, MS onset was decreased, and T I diabetes could be completely inhibited.
  • New testing in humans for IBD showed that some worms could decrease IBD symptoms or cause remission.
  • For the mechanism:
    • They think that the immune response to the worms may be changing the way the immune system works (in the case of the IBD) and that T reg cells may be increased by presence of worms in allergy-resistant people.

[edit] Antibody regulated immune response

  • B lymphoctyes are immoncompeent when they start expressing receptors for a particular antigen,
  • Found in lymph nodes, spleen or other lymphatic tissues.
  • They produce antibodies, the antibodies circulate.
  • B lymphocytes are part of the immune system so they express MHC II proteins and receptors for their antigen.
  • B cells don't hae to chew up their antigen because they have a receptor for it.
  • So when the antigen binds you get a sensitized b lymphocytes.
  • It then interacts with a helper T cell.
  • This allows for the B cell to proliferate.
    • Many will become memory cells.
    • Most become plasma cells.
  • The antibodies generated have the exact same binding site as the antigen-binding protein that is on the surface of the b cell.
  • They can create 2000 ab proteins per cell per second. This can happen for 4-5 days!
  • B cells only generate antibodies to a single epitope.
  • When antibodies bind the antigen, they become a target for complement fixation and phagocytosis.

[edit] Antibodies

  • The antigen binding site is at the very tip and is made by both the light and heavy chains, specifically in the variable region.
  • Part of the constant region of the heavy chain binds complement proteins or for macrophage bidning.
  • Antibodies also have a hinging ability.
  • Lymphocytes can only bind with on antigens.
  • The antigen they can bind to is pre-determined, before the antigen is seen.
  • The variable regions are made up by genes that have many different segments that can get put together to make many different versions.
  • There are also other variations:
    • two different types of light chains
    • 5 different types of heavy chains
  • Types of antibodies:
    • IgG:
      • most numerous,
      • classic structure that we just talked about,
      • the only type of Ab that can cross the placental membrane, and thus confers maternal immunity through placental cross over and breast milk donation.
    • IgA:
      • dimeric, only 15-20% of abs.
    • IgM:
      • pentameric, agglutinate things really well,
      • A, B antigens are these type,
    • IgD:
      • looks like IgG,
      • on B lymphocytes that cause differentiation
      • bound to cells, not free-floating
    • IgE:
      • Same simple structure as IgG,
      • rare, except during an allergic reaction,
      • binds to mast cells, then, next time it sees it's allergen, the mast cells will degranulate.
  • What do Abs do?:
    • They can cause antigens to come out of solution,
    • They can agglutinate cells,
    • They can surround viruses in the blood stream,

[edit] Immunological memory, response time

  • Upon first challenge, IgM shows up in about half a week, with IgG coming just a day later.
  • Second time, IgM is immediate as well as IgG, but IgG's response is way larger in terms of IgG concentration.

[edit] Types of immunity

  • Naturally aquired immunity develops after expsoure to antigens in the environment.
  • Induced active immunity develops after administration of antigen to prevent disease.
  • Natural passive immunity is conferred by transfer of maternal antibodies across placenta or in breast milk.
  • Induced passive immunity is conferred by administration of antibodies to combat infection.
    • Used for rabies or snake bite poisonings.
    • This can generate serum sickness, because one is given the gamma-globulin fraction of WBC extracts from a horse, lets say, in which they produced the antibodies for the antigen.
    • A second exposure can cause system immune response.

[edit] Organ transplantation

  • Biggest successes have been heart and kidney transplantations.
  • The biggest problem is rejection, second largest problem is a lack of organs.
  • The kinds of transplants:
    • Autografts: one part of the body to another, like a bone graft.
    • Isografts: between genetically identical individuals.
    • Allografts: same species, must match at least a 75% match on MHC antigens, will still need to use immunosuppressants.

[edit] Xeongrafts: between different species

  • Most likely is pigs.
  • Primates are ethically challenging.
  • Fetal pig cells are used for Parkinson's and Huntington's disease.
  • Procine islet cells are desireable for diabetes transplants.
  • Pigs are good because:
    • unlimited supply,
    • similar in size and shape,
    • could genetic engineer them to have more human-like MHC profile.
[edit] Wanted-Pig transplants that work
  • Sugars are no good.
    • So we use genetics to get it out.
  • Retroviruses.
[edit] Chimerism and tolerance in a recipient of a deceased donor liver transplant
  • A 9 year old girl was given a liver transplant switched blood group type to become the grouping of the donor.
  • They determined that the HSCs of the donor liver colonized.
  • She needed the transplant because of viral illness.
  • She was O-.
  • Donor was 12 years old.
  • He was O+.
  • They used standard liver transplantation and standard immunosuppressive therapy.
  • She had some bile duct issues and a viral esophagitis and had a small bowel obstruction.
  • They found O+ in her blood stream before surgery.
  • She developed anemia.
    • This was because her RBCs were lysing.
  • She had lots of antibodies going on, she had very high reticulocyte (precursors to the RBCs, normally 3-5%) counts, and she had high levels of auto-antibodies.
  • These generated hemolysis and renal insufficiency (because the complexes build up in the kidney) which required a blood transfusion.
    • So they gave her O-.
  • She got better.
  • 3 Months later, they showed that her lymphocytes were O+, XY!
  • So they believe the blood cells of the transplanted liver moved into the host and wiped out the host cells.
  • This was the first and only case where this is known to have happened.

[edit] Immune disorders

[edit] Allergies

  • Four types:
    • 1: anaphylactic reaction:
      • Doesn't have to go systemic.
      • Allergen is seen, plasma cells generate IgE antibodies, they sit on mast cells. Upon second exposure, antigen binds to antibodies on mast cells, mast cell degranulates (histamines, leukotrienes).
      • Bee stings and penicillin can generate bad reactions.
      • This will cause fluid leaving the blood stream, peripheral dilation, (decreasing blood pressure).
      • Treated with epinepherine which will dilate airways and increase heart rate.
    • 2: Cytotoxic hypersensitivity
      • What you want to happen, except when you're getting a transplant.
    • 3: Immune-complex hypersensitivity.
      • Occurs if you're exposed over and over.
      • This causes large numbers of immune complexes to form faster than phagocytes can clear them.
      • Phagocytes then release contents and destroy tissue.
      • Excess compliment causing release of histamine and an inflammatory response which can lead to glomerular nephritis.
    • 4: Delayed hypersensitivity
      • Shows up well after exposure.
      • Usually occurs with allergens that are typical on the skin.
      • Allergens are taken up by Langerhans cells which are APCs of the skin.
  • Not on exam: Lyme arthritis, the 11 pager.
  • stopped here on 02/04/10.
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