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L#19 & L#20: Effector Responses and Hypersensitivity

by: Denise Croote

L#19 & L#20: Effector Responses and Hypersensitivity 0530

Marketplace > Brown University > Biology > 0530 > L 19 L 20 Effector Responses and Hypersensitivity
Denise Croote
Brown U
GPA 3.9

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The lecture on Effector Responses covers T cell effector functions, Natural Killer cells, the Fas/FasL Pathway and more. The lecture on hypersensitivity covers Type I - Type IV hypersensitivity (a...
Principles of Immunology
Dr. Richard Bungiro
Class Notes
Effector Responses, Hypersensitivity, immunology
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This 4 page Class Notes was uploaded by Denise Croote on Saturday January 23, 2016. The Class Notes belongs to 0530 at Brown University taught by Dr. Richard Bungiro in Fall 2013. Since its upload, it has received 15 views. For similar materials see Principles of Immunology in Biology at Brown University.

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Date Created: 01/23/16
Lecture Nineteen: Effector Responses  B cell effector functions: the Fc receptor of the antibody is very important to the antibodies effector functions. The Fc receptor can…. o bind to the macrophage and opsonize it for phagocytosis o bind complement and partake in the MAC complex formation and following lysis o bind NK cells to activate antibody dependent cell mediated cytotoxicity and resulting apoptosis o Fc receptors are covered in ITAMS for signaling  T cell effector functions: o Peptides that bind the MHCII activate Th1 and Th2 cells. Th1 cells activate CTLs which eliminate self altered cells and Th2 activate B cells o Peptides that bind to MHCI activate CTLs which eliminate altered self  Properties: o Less stringent activation requirements than naïve cells, reduced need for co-stimulation o Increased expressing of cell adhesion molecules o Different trafficking patterns in that they can enter inflammatory sites o Express effector molecules like soluble cytokines and cytotoxins o Have membrane bound effector molecules (like FasL for apoptosis induction)  Generation of CTLs o Generated from CTL precursors o Activation of CTL precursors requires foreign antigen presentation by DCs o Occurs through a class I MHC pathway o CD4 Th cells are usually necessary for licensing the DC (making it able to present) before the DC can activate the CTLp o Memory CTLps require less IL2, may not require CD28 and B7 interaction and may not require help from Th cells o You also make CTLps after you activate CLTps. You would not want memory CTLs because they would be active all of the time  To activate naïve T cells you need o 1.) TCR to bind to MHC class I/peptide complex o 2.) CD28, and B7 costimulation o 3.) IL2 cytokine signaling  To activate effector CD8 T effector cells you only need 1 signal and that is TCR engagement with the MHC and peptide complex  CTL Killing Activity: o Perforin/Granzyme Pathway: 24-58 hours after activation CD8 T cells produce granules containing perforin ( a pore forming protein – bad because the good contents of the cell leak out and the bad contents of the cell rush in) and granzyme (which have apoptotic inducing effects)  CTL and target cell form the conjugate  CTL undergoes cytoplasmic rearrangement  CTL exocytoses the granule  CTL and target cell dissociate, the target cell dies and the CTL moves on to kill another cell o Fas/FasL Pathway: the FasL ligand is found on the surface of the CTL and it binds to Fas expressed on target cells and induces apoptosis o CTLs produce IFNy  Direct antiviral effects, activates macrophages, increased expression of class I MHC leads to increased antigen presentation and promotes Th1 CTL activating responses  Natural Killer cells (NKs) – component of the innate immune system, their function is regulated by a balance between activating and inhibiting receptors and innate cytokines o Highly cytolytic and they produce cytokines very early during the immune response o Their peak activity is right after viral infection o NK cells produce INFy o Use the perforin/granzyme pathway to kill CTLs o Can lyse antibody coated cells via Fc receptor binding (ADCC) o Viruses down-regulate class I MHC, need class I MHC to bind and inhibit the NK cells, without MHC I the NK cells are given the go ahead to kill o NKs buy you time so that you can generate CTLs but still fight the pathogen during this lag period  ADCC – multiple cells with cytotoxic potential express receptors for Fc regions (like NK cells, monocytes and macrophages, eosinophils, neutrophils. ADCC is often used to kill things that are too big to phagocytose (parasites)  The ability to bind to Ab Fc receptors shows some kind of specificity  ADCC kills multicellular parasites by releasing TNF, lytic enzymes, perforin, and granzymes  Mixed Lymphocyte Reactions: o Takes 24 to 48 hours for T cells to proliferate o Take 72-96 hours for a functional CTL population to be generated o One population is rendered unable to proliferate while the response of the other is measured (populations differ in MHC haplotype)  If the differences in MHC is large there will be a large proliferation of one CTL population  Proliferation of the one T cell population can be measured with 3H thymidine incorporation o Graft vs. Host disease is an example of this – the graft MHC rejects the host MHC and begins to attack the host. The host has no immune system to fight back because it was wiped out during the radiation Lecture Twenty: Hypersensitivity  Hypersensitivity is incidental tissue death, self cells are caught in the cross-fire of immune response, happens when the immune response becomes excessive or inappropriate  Immediate reactions are Type I,II, and III (and are mediated by antibodies) and delayed reactions are type IV (and are mediated by T cells)  Type I Hypersensitivity: o Takes minutes to induce o May be local or systemic o Is a response to allergens (like food and bee stings) o Induce a Th2 response which leads to the production of IgE o IgE binds to mast cells and basophils via the Fc receptor and this cross linking causes degranulation and release of inflammatory mediators (histamines) from mast cells o Pathway: allergen binds to a B cell, B cell is activated by a Th2 cell, differentiates into a memory and plasma cell, plasma cell secretes allergen specific IgE, IgE binds to sensitized mast cells and degranulates them o Mast cells release histamines that lead to smooth muscle contraction, vascular permeability, and mucus secretion o Cytokines stimulate IgE production and mediate shock o The end result is nerve damage, inflammation, tissue remodeling, and acute change in function  Mast cells have high affinity receptors for IgE while B cells and macrophages have lower affinity receptors  Mast cells can also be activated by drugs that increase Ca+ uptake and C3a and C5a  Anaphylaxis – smooth muscle contraction that leads to bronchiole constriction and edema, blood pressure crashes, must be treated with an EpiPen immediately, is a systemic reaction  Can also have localized reaction like in the lower respiratory tract (asthma), vomiting and diarrhea (reaction to food allergies), skin hives, and dermatitis  Immediate reactions occur within minutes and are caused by histamine release, late phase reaction occur within six hours and represent a more diffuse swelling resulting from infiltration by Th2 cells and macrophages  Chronic asthma is a result of excessive mucus production that thickens the bronchial walls and make it hard for air to travel through  Anytime you see dots on a tissue scan it mean inflammation  IL4 increases IgE production and IFNy decreases IgE production  Can diagnose an allergy with a RIST test (tests the amount of IgE to see if there is an increase in the amount of IgE present – meaning you are allergic to something) or can use a RAST test (which tests for the amount of IgE present in response to a specific allergen)  You can treat a Type I reaction with avoidance, hyposensitization, monoclonal anti-IgE, antihistamines, and epinephrine  Type II Hypersensitivity: Antibody Mediated Cytotoxicity – mediated by autoantibodies plus C’ via ADCC o Takes -8 hours to induce o Mediates transfusions and drug induced anemia o Happens during pregnancy – if the mother is Rh- and the baby is Rh+ the first pregnancy will be okay, but during the delivery some of the baby’s blood will get into mom and mom will make IgG antibodies for the positive, the next time she is pregnant these antibodies will travel across the placenta and go after the baby’s blood and kill the baby. This is avoided with Rhogam shots. o Rhogam shots prevent B cell activation and memory B cell formation  Type III Hypersensitivity: Immune complex mediated – immune complexes activate complement, leading to the degranulation of mast cells and release of inflammatory mediators o Results in tissue damage from the release of lytic enzymes from recruited neutrophils o Reactions are often specific to certain tissues ex.) arthritis o Happens 4 to 6 hours after exposure if antibodies are already present o Doesn’t happen during the first exposure, happens after the second exposure o You might get serum sickness if you are injected with horse Ab because of the differences in haplotype  Type IV Hypersensitivity (Delayed Type Hypersensitivity = DTH): is mediated by Th1 cells which secrete cytokines and activate macrophages that attempt to clear or wall off the offending antigen o Typically takes 24 to 72 hours to induce o APC presents the antigen to a CD4 Th cell which generates Th1 o Th1 secretes cytokines and activated macrophages o Can cause granulomas to form, granulomas are cellular balls that wall off a pathogen o Granulomas often form around parasites because parasites are bigger o An example would be a response to Poison Ivy, Oak  Penicillin can induce all of the type hypersensitivity reactions o Can induce anti-IgE which can lead to anaphylaxis o Can bind host RBC are cause them to be lysed by anti IgG or IgM o Can lead to immune complex formation and complement activation o Can activate anti penicillin Th cells Review Chart Type I Type II Type III Type IV Induced By Allergens Bound antigens Soluble antigens Souble antigens Mediated By IgE IgG and IgM IgM and IgG Th1 cells Mechanism Mast cell Death by ADCC or C’ Immune complex Macrophage degranulation and activation formation and lysis destruction histamine release Time Frame 2-30 minutes 5-8 hours 4-6 hours 24-72 hours


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