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46 Cards in this Set
- Front
- Back
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Antigens |
Foreign or unexpected molecules. Molecules that stimulate an immune response Most antigens are proteins, but other molecules can trigger a response as well |
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Innate Responses |
Present at birth and provide protection from common pathogens 1. Generally Rapid 2. Stereotyped 3. Short Term 4. Directed at common pathogens and damaged tissue |
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Adaptive/Aquired Responses |
Develop over time, provide long lasting immunity once developed. 1. Slower 2. More developed 3. Extremely Flexible 4. Long-Term Protection |
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Antigen Receptors |
Receptors on immune cells which bind to foreign material with high affinity and initiate intracellular signaling events. |
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Inflammatory Signals |
Produced once an antigen or tissue damage is detected and both immune and non-immune cells broadcast the inflammatory signal. 1. Cytokines-Act by long distance 2. Cell Surface Components |
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Effector Functions |
Attack of pathogen, and removal of damaged or altered host tissues by immune cells. Autoimmune disease occur when there is a problem with this pathway |
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Innate Receptor Genes |
Present in the Germline DNA 1. Toll-like Receptors (TLRs): Important family of receptors. 2. Specific for pathogen components: Lipopolysaccharides of bacteria |
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Innate Receptors |
Recognize constant reatures specific to pathogens. PAMPs: Pathogen Associated Molecular Patters Ex. Lipopolysaccharides (LPS), dsRNA, Unmethylated CpG DNA, N-formyl methionine in proteins. |
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Toll-Like Receptors |
Innate and present in germ line DNA. Produced by billions of years of evolution Recognize things that would indicate non-self molecules |
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Aquired Receptor Genes |
Not Present in Germline DNA, but created by molecular mechanisms that rearrange the receptor genes 1. Highly variable and unpredictable 2. Each immune cell may have a different antigen receptor 3. Can occasionally bind self, and are responsible for allergies and organ rejection ***Immunce cells that work effectively will divide to reproduce, but this takes time |
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Adaptive Pathogen Receptors |
1. Only in vertebrates 2. Created by genetic rearrangements and mutation during lifecycle 3. Not Present in Germline DNA Created by rearrangement in lymphocyte cells as they are developing |
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Innate Immune: Cells |
1. Macrophages
2. Granulocytes 3. Natural Killer (NK) Cells 4. Antigen-Presenting Cells (APCs) 5. Epithelial Cells (Paneth)=Defensins *Interferons (Class of Cytokines) produced by cells of immune system. |
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Cytokine Signaling |
Cytokines= Low Molecular Weight Glycoproteins 1. Produce by immune and non-immune cells 2. Regulate immune responses of innate and adaptive 3. Regulate host response to infection... Fever... 4. Regulate Hematopoiesis (CSFs) ***Cytokine Storm: Misregulation of cytokine resulting in serious pathologies |
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Macrophages and PMN Recruitment |
1. Macrophages recognize infection and release chemokine (CXCL8) 2. CXCL8 activates integrins on PMNs (increasing adherence to wall of capillaries near infection) 3. PMNs enter tissue and phagocytose bacteria. 4. PMNs recognize bacterial products and bind to antibodies on bacteria. |
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Interferon Signaling |
One cell gets infected, it will notice it is infected (toll receptors) and express interferon to affect neighboring cells to increase resistance to infection by viruses.
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Innate Immune: Complement |
*Complement is a set of serum proteins produced by the liver and serves numerous important innate functions. Ex. C3b= fragment of protein that covalently attaches to surfaces of pathogens. 1. Opsonins (C3b): Molecules that mark targets for immune reactions (phagocytosis) 2. Membrane Attack Complex (MAC): Other complement proteins which allow for attack which can lyse cells |
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C3b and MAC Deficiencies |
C3b is a protein fragment which covalently attaches to the surfaces of pathogens and serves as part of an enzyme that stimulates the addition of more C2b. It is an Opsonin. C3b Deficiency: Increased risk of a variety bacterial infections MAC Deficiency: Increased frequency of infections by Neisseria Bacteria |
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Paroxysmal Nocturnal Hemoglobinuria |
Autoimmune disease in which C3b is not removed from host cells and are therefore attacked. This can happen on RBCs causing them to lyse and resulting in Paroxysmal Nocturnal Hemoglobinuria. |
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Lymphoid Progenitor Cell |
Gives Rise to Pre-T and Pre-B Pre-T become Naive T cells in thymus Pre-B become Naive B cells in Bone Marrow |
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Naive Cell |
1. Has receptor but has not encountered antigen 2. In blood, lymphatics, and peripheral lymphoid system 3. Encounter with antigen leads to activation |
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Lymphocyte Overview |
1. B and T Cells 2. Have surface antigen receptors (B and T Types) 3. Antigens bind receptors 4. All receptors are the same on a cell, but each cell is different |
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Antigen Receptor Signaling: Stop or Go |
Stop: Die (Clonal Elimination), Become Innert (Clonal Anergy) Go: Divide= Clonal Selection by antigen |
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Effector and Memory Cells |
1. Effectors do something about antigen 2. Memory cells are pre-selected pool for rapid response if antigen reappears. |
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What are the pro's and con's of aquired immunity? |
1. Pro= Produce billions of different antigen receptors to respond to various antigens. Antigen then selects for the proper effector cell 2. Con= Self-reactive receptors will be generated, autoimmune diseases. |
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What basic biological process does the production of memory cells resemble? |
Natural Selection |
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Antigen Presenting Cells |
Not Lymphocytes but Born in the Bone Marrow. These present antigens to lymphocytes 1. Professional= B cells, macrophages, dendritic cells (Class II MHC) 2. Non-Professional= all cells in human body other than RBCs (Class I MHC) |
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B Cells, B= Bursa |
1. Born in the bone marrow 2. 5-25% of circulating lymphocytes (1 month) 3. Give rise to plasma cells which make antibodies 4. Effector= plasma cells secrete immunoglobulin (Ig) molecules |
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Humoral Immunity |
Humor=Blood or Body Fluids 1. Opsonize= binding of antibody to molecule, granulocytes or macrophages see these molecules then attack 2. Neutralize= Antibodies neutralize viruses and bacteria and prevent entry into host cells |
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T Cells= Thymus Dependent |
1. 65-75% of circulating lymphocytes 2. Live for years 3. T-cell antigen receptor can only see antigen presented on another cell's Major Histocompatibility Complex Molecule (Integral Membrane Proteins) 4. Effector: Th, Tc, Treg |
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Types of T Cells |
1. Th= Helper T Cells, CD4 cells which secrete cytokines and coordinate immune activity 2. Tc= Cytotoxic T Cell (Killer T Cell), CD8 cells which kill cells 3. Treg= Regulatory T cells, Subset of CD4 cells which are involved in suppressing immune activities |
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Th Cell Effect |
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Th Additional Activites |
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Tc Killing Cells |
1. Tc cells, run into target cells which present antigens by the MHC protein complex. This will allow an attack to occur. |
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How Tc Cells Kill |
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T reg Cells |
1. Suppress immune response especially self-reactive T cells 2. Target of clinical interest a. turn on for transplants and autoimmune disease b. Turn off for tumors and vaccines |
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Antigen Presentation
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1. Antigen Presenting Cells (APCs) present antigens to lymphocytes |
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Antigen Presenting Cells
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1. Present Antigens to lymphocytes and supply cytokines 2. Bind antigens in periphery, become activated, and move to lymph nodes (Then are called dendritic cells) |
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Follicular Dendritic Cells
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Present antigens to B cells in the lymph nodes.
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Professional APCs
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1. B cells, macrophages, and dendritic cells present to T cells
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Presentation to B Cells
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1. Follicular Dendritic Cells in lymph nodes trap and present antigens to B cells 2. Some antigen processing occurs 3. FDCs provide cytokines to attract B cells and promote survival |
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Presentation to T Cells
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1. Most antigens seen by T cells are proteins 2. Proteins cut into small peptides and bound to MHC molecule which is put on cell surface 3. T cell receptor (TCR) can see peptide antigen displayed by MHC 4. Naïve T cell must be antigen and MHC molecule in order to become activated |
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TCR Seeing Antigen and MHC
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MHC Class II: peptides presented to CD4 MHC Class I: Peptides presented to CD8 (All cells in body other than RBCs) |
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MHC Restriction
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1. T cell Receptor must see host MHC and Antigen Presented: T cells restricted to seeing antigen on particular MHCs a. Most Th cells are restricted to MHC Class II b. Most Tc cells are restricted to MHC Class I ***Only professional antigen presenting cells express MHC Class II |
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Class I and II MHC Presentation
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Naïve T Cell Activation by 2 Signals
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1. MHC with antigen 2. B7 on APC binds with CD28 on Naïve T cell. (Second Handshake) ***This causes T cell to express Interleukin2 which stimulates clonal expansion |
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Tc Activation
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Cells infected by virus cut up viral protein (proteasome), bring it into rough ER by Transporter of Antigen Peptides (TAPs), then binds peptides to MHC class I molecules to present. An Activated CD8 T cell (Tc or CTL) will see this and release cytotoxic factors to kill the cell |
