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84 Cards in this Set
- Front
- Back
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What are the two main divisions of the immune system? |
Innate and adaptive |
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Describe the innate immune system |
Protects a naive animal (an animal that has not previously exposed to a pathogen), protects immediately, not antigen specific, responses to danger signals from microbes (PAMPS) or damaged tissues (DAMPS), provide signals to adaptive immune system |
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What are the 5 components of the adaptive immune system? |
Barriers, phagocytic and sentinel cells, complement, cytokines, and NK lymphcyte cells |
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Adaptive immune system |
Develops after exposure to an antigen, required days to weeks to develop (typically 7-10 days at least), antigen specific and expandable, has memory, has tolerance, enhances the innate response through cytokines, has two components (humoral [B cells/antibody] and cell mediated [T cell mediated]) |
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Do the innate and the adaptive immune system communicate? |
YES! Communication between the two are important for a successful response |
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5 major components of innate immunity |
Barriers, phagocytic cells and sentinel cells, complement system, cytokines, and NK (natural killer cells) |
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Barriers to infection |
Intact skin and mucous membranes (epithelial barriers), acid in stomach, mucous on surfaces that provide protection, antimicrobial peptides (defensins, these are small proteins that poke holes in some bacteria and kill them) |
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What are defensins? |
Small molecular weight proteins that are found along epithelial surfaces. These small proteins poke holes in some bacterial cell membranes... These are considered part of the barrier part of the innate immune system |
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Phagocytic and Sentinel cells |
Are important for ingesting and killing pathogens (neutrophils and macrophages). |
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Complement System |
Series of 20 - 30 proteins in the blood plasma. An enzyme cascade system that has antimicrobial activity, very rapidly induced, multiple mechanisms for controlling microbial infections. Potent! If it is induced and not regulated the result is DEATH! |
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Innate defense cytokines |
Protein messenger molecules produced by stimulated cells; the cytokines act on the cells that produced it, nearby, or far away! There are 3 different kinds of cytokines (pro-inflammatory cytokines, chemokines, and interferons). Cytokines are produced by many different cell types. |
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What are the 3 types of cytokines? |
Pro-inflammatory cytokines (Interleukin 1, IL6, and TNF) |
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NK (Natural Killer) Cells |
Non antigen specific lymphocytes, important for killing virus infected cells and tumor cells, targeted to cells that do not express normal proteins (MHC1), EXPRESS YOURSELF OR DIE, cells expressing stress proteins, and/or cells with antibody bound to them. |
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Summary of Innate Immunity |
Fairly efficient and works most of the time, no memory, extremely important first line of defense, can be suppressed by crowding, stress, cold temperatures, etc. Can work independently of adaptive immunity but function is enhanced by adaptive immunity by making the components of innate defense even more powerful |
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What are the two major components of the adaptive immune system?
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Humoral (antibodies) and cell mediated (t cells) |
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Humoral Immune System |
B cells produce antibodies and antibodies provide humoral immunity. |
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What are the classes (isotypes) of antibodies? |
IgM, IgG, IgA, and IgE can be secreted! Very small amounts of IgD are secreted and are poorly defined function wise because FU |
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What is the function of IgM? |
IgM - First antibody produced in every response and largest molecule. Functions in blood stream with short half life |
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What is the function of IgG? |
High in serum, important in systemic diseases in general, second antibody produced |
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What is the function of IgA? |
important on mucosal surfaces as a dimer |
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What is the function of IgE |
Important in allergies and in parasite infections; found on mast cells; very little in serum under normal circumstances |
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What is the function of IgD? |
Major roll as a B cell surface receptor and is co expressed on the surface of mature naive B cells |
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What is cell mediated immunity? |
Named because the transfer of immunity from a protected animal to a susceptible animal involves the transfer of cells. |
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What are the two main divisions of cell mediated immunity? |
Alpha beta T cells (lymphocytes) -> (CD4+ which are T helper cells and CD8+ which are cytotoxic T cells) |
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What are CD4+ ? |
T helper cells! Produce cytokines that regulate both the innate and adaptive immunity mechanisms. Important for directing which antibody class is produced! |
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What are CD8+? |
Cytotoxic T cells, or Cytotoxic T Lymphocytes (CTL). These attack and kill cells that makes foreign protein, eg. viral infected cell or tumor cell |
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What do gamma delta T cells do? |
Protection at mucosal surfaces??? Still more to be discovered if anyone feels like casually gettin' famous |
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Explain antibody recognition? I guess |
Antibodies recognize a small portion of a molecule (EPITOPE), which is only about 6-8 amino acids long, and are very specific. 10^9 different epitopes recognized by B cells |
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How do B cells and T cells differ in their epitope recognition? |
B cells recognize intact antigen (not processed); the 3D structure is important, recognize proteins, lipids, carbohydrates (yum), etc. |
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How many types of MHC molecules are there, and how do they differ? |
MHC1 is a surface molecule on all nucleated cells and presents antigen to CD8+ T cells |
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What are two really cool features of the adaptive immune system? |
Memory and Tolerance! |
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Cool facts about the memory part of the adaptive immune |
It occurs on re-exposure to an antigen. It is faster than primary response, antigen specific clones of B lymphocytes have expanded and matured. The antibody produced in secondary is higher titer, higher affinity, and class switching has already occured from IgM. |
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Cool stuff about Tolerance (justin trudeau save us) |
The adaptive immune system tolerates (doesn't attack) self molecules. Antigens presented during lymphocyte development recognized as self, those presented after development recognized as foreign. |
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List some examples of what can happen during immune system dysfunction |
Hypersensitivities (like yo biitch azz), autoimmune disease, and immunodeficiencies |
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Where do blood cells originate and list them |
Orginiate in the bone marrow: platelets, RBCs, and 5 WBCs (basophils, eosinophils, monocytes, neutrophils, and lymphocytes) |
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What does a basophil do? |
Makes up 0.5% of WBCs in circulation, contains granules filled with inflammatory mediators, important in allergies and parasites (secondary to eosinophils) |
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What does an eosinophil do?
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1-3% of WBCs in circulation, half life of 30 minutes. Contains granules filled with potent mediators capable of killing parasites! Important in extracellular control of parasites. Circulate 30 min then go under epithelium live couple weeks. |
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What's up with monocytes? |
3-7% of WBC's in circulation. Circulate 1-2 days than migrate into tissues and differentiate into a macrophage. Macrophages have different functions depending on the tissues they're found in. Important in phagocytosis and killing of bacteria and presentation of antigen on MHC2, and secretion of cytokines. Accumulations mean chronic inflammation |
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Neutrophils! |
55-90% of circulation WBCs! Highest, duh because numbers. Short lived cell, survive 1-2 days at most. About 2.5 times a day all replaced. Important against bacterial infections! First responders! Substantial numbers within 4 hours, and bone marrow increases production! Neutrophilia = bacterial infection. Neutropenia = viral infection. Attack and destroy bacteria, killing self in the process |
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Lymphocytes, bitchhhh |
About 30% WBCs in circulation. Made up of B cells, T cells, and NK cells. Circulate around 4 months between blood and lymphoid tissue looking for antigen. Naive B cells and T cells are morphologically the same. If contact antigen, they are activated, undergo mitosis, and then differentiate into memory cells, which continue to live. |
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Where are endothelial cells? |
They line the blood and lymph vessels |
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Why are endothelial cells important in the immune system? |
Important for signaling cells and regulating leukocyte traffic in tissue. Have adhesion molecules known as addressins that allow circulating leukocytes to know where they are. Addressins can be upregulated and downregulated. During an infection, they will be upregulated and allow circulating neutrophils to bind and diapedese to site of infection |
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Myeloid cells and their maturation |
Under normal circumstances, neutrophils, esosinophils, and basophils are released in a mature state. Dendritic cells mature in tissue, mast cells mature in tissues. |
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Lymphoid cells and their maturation |
T lymphocytes and B cells are released as immature and need to go and mature before they're effective. NK cells are released ready for action! |
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T lymphocyte maturation |
T lymphocytes are released from the bone marrow as pre-T cells. They then travel to the thymus (primary lymphoid tissue) to mature. An antigen receptor (TCR) is generated by DNA rearrangement, if it recognizes the thymus that cell is eliminated. If it recognizes an MCH molecule but doesn't recognize thymus, then the T cell matures and goes to secondary lympoid tissue. |
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B cell maturation |
Released immature from the bone marrow as Pre-B cell and go to primary lymphoid tissue (species specific), where it develops its antigen receptor (BCR). If passes test, then goes to secondary lymphoid tissue! |
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What happens in secondary lymphoid tissue to mature naive B and T cells? |
Clonal expansion! The expanded clones then differentiate. B cells differentiate into effector cells called plasma cells (secrete antibody) or memory cells (long lived clones). Helper T cells (CD4) differentiate into effector cells and memory cells cytotoxic t cells differentiate cytotoxic and memory cells. Gamma delta effector or memory. PATTERN OMG. |
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All about primary lymphoid tissue! |
Function: maturation of lymphocytes following exodus from the bone marrow. For T cells, it is the thymus. For B cells it is species specific! In birds, bursa of fabricius; in some species, it is the bone marrow, in other, ileal Peyer's patches. |
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All about secondary lymphoid tissue! |
Function: increase the chances that a lymphocyte meets its antigen... Large numbers of lymphocytes are in secondary, just waiting for their antigen. Lymph nodes, spleen, MALT! Most are in lymph nodes, then bone marrow, intestine and spleen.... ONLY 2% IN BLOOD |
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Are most WBC's in the blood? |
NO! Only 2% of the lymphocytes in the body are in the blood |
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Can we tell T cells and B cells apart on a slide? |
No, if not responding to antigen, they don't have much cytoplasm and many organelles are NOT able to be told apart from light microscopy. |
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What lymphocytes makes up the majority in the circulating blood? |
T cells, at 75%. All have CD3 (cluster of differentiation) and TCR. Types of T cells differ based on their TCRs. B cells make up around 15-20% of the lymphocytes circulating. BCR, which is Ig with transmembrane anchor. NK cells 5-10% |
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How do B cells recognize an antigen? |
Recognize unprocessed antigen via its BCR, which is a membrane bound antibody molecule. CD79 = signal transduction molecule |
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How do T cells recognize an antigen? |
Recognize protein antigen presented on MHC molecule via the TCR. CD4 recognizes MHC2, CD8 recognizes MCH1. CD3 molecule signal transduction |
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What is tetanus and what does it cause? |
Caused by a neurotoxin produced by Clostridium tetani, gram positive anarobic bacteria. Spores of which are found in soil, feces, etc. Horses and humans are particularly sensitive to the toxin. Associated with deep puncture wounds. Rigid paralysis. |
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What happens during Clostridium tetani infection? |
Bacteria introduced via a wound, anarobic environment develops in necrotic tissue, replicate and produce toxin, immune system stimulated! |
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Describe the acute inflammation response of Clostridium tetani |
Tissue damage and stimulation of sentinel cells by PAMPs lead to release of factors (including proinflammatory cytokines) which cause upregulation of adhesion molecules and increased vascular permeability, influx of neutrophils and exudate, phagocytic cells phagocytize and try to kill bacteria, but not all are killed |
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How long will an adaptive immune response take in a naive animal? (at best) |
7-10 days! |
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Will the adaptive immune system be able to help during a Clostridium tentani infection? |
Probably not, by the time antibody levels rise enough, enough of the toxin from the bacteria will be made in order to cause rigid paralysis in the affected animal |
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How do we control and prevent tentanus? |
Antibiotics to kill the bacteria, antitoxin (IgG to tetanus toxin) to neutralize it, and Tetanus toxoid (inactivated toxin which stimulates active immunity). |
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What happens in an animal that has been vaccinated for tetanus |
Clostridium tetani are introduced into a wound and they begin to replicate and produce toxin, acute inflammatory phase begins as normal, the animal already has IgG to the toxin and it will be in the exudate that leaks to the injury, IgG will bind to the toxin and neutralize it. Vet arrives, cleans wound to rid of bacteria, antibiotic to kill bacteria, and tentatus booster to increase titer of IgG. |
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Introduction to neutrophils |
Phagocytose and kill bacteria, first responders! Predominant WBC in circulation, circulate 8-10 hours then migrate to tissue and live 1-2 days. Adult human makes 100 billion per day. Part of innate immune system, doesn't require previous antigen exposure. High numbers in acute inflammation |
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What is an abscess? |
Dead and dying neutrophils and tissue cells. Neutrophils will clean up after themselves and accumulate in abscess, can rupture to surface. Enzymes from neutrophils breaks down tissue |
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Neutrophil structure |
Condensed DNA, Glycogen granules (storage form of glucose, used for energy through anaerobic glycolysis), also contains primary and secondary granules (carry bactercidal substances and substances to digest tissue), extra cell membrane for phagocytosis and motility, receptors important! cell adherin molecules, antibody receptors and inflammatory mediator receptors |
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Neutrophil phagocytosis |
Neutrophils can phagocytose anything more hydrophobic than itself! The neutrophil membrane receptors important in phagocytosis, Fc receptors bind antibody bound to an antigen, especially IgG antibody. C3b receptor bind to c3b when it is coating a bacteria. Opsonization. |
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Steps of phagocytosis |
Attachment, engulfment, formation of a phagosome, then phagolysosome |
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Example of bacterial interactions with neutrophils |
Because bacteria can only phagocytose bacteria more hydrophobic bacteria, they need to coat bacteria with either antibody or C3b. Like Staph. Mycobacteria are different, where they are easily phagocytosed but then resist killing! |
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3 Step Neutrophil Killing Process |
1) lytic enzymes and antimicrobial peptides from primary and secondary granules 2) oxidative metabolism [respiratory burst] 3) neutrophil extracellular traps [NETs] |
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Primary granules contain what? |
Lytic enzymes and antimicrobial peptides! Primary granules contain hydrolases, lysozyme (break down peptidoglycan in gram positive bacteria), defensins (small proteins that kill bacteria from making pores. Hydrophobic outside and hydrophillic interioer, like MAC of complement. Insert into a membrane make a pore), myeloperoxidase (an enzyme that has an important roll in oxygen mediated killing mechanism |
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Secondary granules contain what? |
Lysozyme, lactoferrin (chelates iron, harming bacteria), collagenase (degrades connective tissue so that the neutrophil can move through tissues) |
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What is the most potent killing mechanism of a neutrophil? |
Oxidative burst! This occurs within the phagolysosome. Products include: hypochlorite, hydrogen peroxide, aldehydes, and oxygen radical! |
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Neutrophil extracellular traps or NETs |
Stimulated neutrophils barf up nuclear material and granular proteins extracellularly, which creates a mesh that traps bacteria and the antimicrobial proteins kill the bacteria... This is an active response to inflammatory stimuli, this is called NETosis... |
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Under what circumstances do neutrophils functions decrease? |
Distress (glucocorticoids), some viral infections, bacterial virulence factors, neonates, periparturient period |
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Under what circumstances do neutrophil functions increase? |
Innate defense cytokines, complement products that are released within hours of infection stimulate neutrophils, helper T cells produced within 7-10 days also stimulate. |
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How do neutrophils move through the blood? |
Through loosely binding to endothelium via selectin adhesion molecules and roll along, called margination! Fear, epinephrine, and glucocorticoids cause demargination and leukocyte numbers increase in circulation, this is called a stress leukogram! |
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How do neutrophils leave the blood stream to attend to an infection? (4 steps) |
Rolling: selectin mediated loose binding of neutrophil to post capillary venules |
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What other leukocyte are eosinophils most similar to? |
Similar to neutrophils but not as good at phagocytosis. Use exocytosis instead |
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When are eosinophils stimulated? |
During IgE mediated allergies and during parasitic (esp. extracellular) infections |
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What are the functions of eosinophils? |
To attack really big things (like parasites) and to circulate in the blood for 30 minutes before leaving and concentrating under epithelial surfaces |
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How does an eosinophil move? |
Similar to neutrophil, with diapedesis and chemotaxis. Unlike neutrophils, they bind to Fc portion of IgE with their Fc epsilon receptor area |
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How do eosinophils kill? |
Damaging products are released outside, lysosomal contents emptied onto surface of the parasite cuticle, produce oxygen radicles on parasite surface. |
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How are eosinophils activated? |
Cytokines! Specifically from Th2 cells and macrophages! |
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What is Bovine Leukocyte Adhesion Deficiency? |
Autosomal recessive, genetically inherited trait of Holsteins that results in a defective integrin molecule. |
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What happens in a calf with BLAD? |
Neutrophils are unable to bind tightly and therefore can not diapedese out. This causes neutrophilia inside of the bloodstream |
