Chapter-22 Immune System and Body Defense Flashcards

(89 cards)

1
Q

Infectious Agents

A

Organisms that cause damage or possible death

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2
Q

Pathogenic

A

Infectious agents that cause harm to a host

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3
Q

Bacteria

A

Prokaryotic

Intracellular and extracellular parasites, produce enzymes, toxics

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4
Q

Viruses

A

Not cells, composed of DNA or RNA within a protein capsid, or shell.
Obligated Intracellular parasites, must enter a cell to replicate

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5
Q

Obligate Intracellular Parasites

A

Must enter a cell to reproduce or replicate

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6
Q

Fungi

A

Eukaryotic
Produce pores, release proteolytic enzymes
Exp–> yeast, molds, ringworm, diaper rash, athlete’s foot

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7
Q

Protozoans

A

Eukaryotic cells, Lack cell wall

Exp–> Malaria, toxoplasmosis, African sleeping sickness, giardiasis

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8
Q

Multicellular Parasites

A

Eukaryotic,
Live within a host, grow in size with nutrients provided by host
Exp–> tapeworms, lung flukes, liver flukes,

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9
Q

Prions

A

Small fragments of infectious proteins that cause disease in nervous tissue
Exp–> Mad cow disease, getting it by consumption of infected cow meat, make your brain spongy

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10
Q

Structures that House Immune System Cells:

Lymphatic Tissue

A

T-lymphocytes, B-lymphocytes, Macrophages, NK cells are housed in secondary lymphatic structures: spleen, tonsils, malt, lymph nodes, lymphatic nodules

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11
Q

Structures that House Immune System Cells:

Select Organs

A

Macrophages are housed in other organs, named based on location: alveolar macrophages of lungs, microglia of the brain
Either Permanent Residents=Fixed Macrophages, or Migrate through tissues=Wandering Macrophages

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12
Q

Structures that House Immune System Cells:

Epithelia Layers of the skin and Mucosal membranes

A

Dendritic Cells are located skin, mucosal membranes
Derived from monocytes like macrophages.
Dendritic cells engulf pathogens of the skin and mucosal membranes and migrate to lymph node

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13
Q

Structures that House Immune System Cells:

Connective tissue

A

Mast cells are located in the CT through the body

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14
Q

Structures that House Immune System Cells?

A
  • Lymphatic Tissue
  • Select Organs
  • Epithelial Layers of skin and mucosal membranes
  • Connective Tissue
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15
Q

Cytokines

A

Small soluble proteins produced by cells and released to bind to specific receptor of target cell
- Regulate and facilitate immune system activity
Exp–> Interlukin
Tumor Necrosis
Colony-stimulating Factor
Interferon

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16
Q

Innate Immunity

A

Born with these defenses

  • 1st line of defense
  • Barriers of skin, mucosal membranes that prevent entry,
  • Physical barriers epithelial tissue of the dermis,
  • Chemical barriers, release antimicrobial substances(cells release IgA, lysozyme sebum), biological barriers (normal flora)
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17
Q

Adaptive Immunity / Acquire Immunity

A

Involves T-lymphocyte and B-lymphocytes which respond to different foreign substances (antigens) which we are exposed during lifetime

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18
Q

Cellular Defenses:

Neutrophils and Macrophages

A

Neutrophils - 1st to arrive during inflammatory response
Macrophages - are in tissue through the body
Both engulf unwanted substance such as infectious agents and cellular debris through phagocytosis
Engulf-Lysosome+Phagosome=phagolysosome (destroys infectious agent)

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19
Q

Cell Defenses:

Basophils and Mast Cells

A

Basophils - circulate the blood
Mast cells- Reside in Ct of skin, mucosal lining and internal organs
Serve as chemotactic chemicals
Release granules during inflammatory response: Histamine, Heparin, Ecosanoids

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20
Q

Histamine

A

Increases Vasodilatation and increases capillary permeability

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21
Q

Heparin

A

Anticoagulant

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22
Q

Ecosanoids

A

Release from plasma membrane with increase inflammation

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23
Q

Cellular Defenses:

Natural Killer Cells

A

Destroy a variety of unwanted cells including viruses, bacteria, tumor cells, transplanted tissue
Release cytotoxic chemical perforin and granzyme
Perforin forms a transmembrane pore (hole) and granzyme goes in cell causing apoptosis

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24
Q

Immune Surveillance?

Where are they found?

A

NK cells patrol the body in an effort to detect unhealthy cells, Found in red bone marrow, blood, and secondary lymphatic structures

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25
Eosinophils
- Target parasites by degranulation and releasing enzymes and other substances lethal to parasites. - Release proteins that form transmembrane pore to destroy multicellular organisms. - Participate in immune responses: allergies, asthma
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Antimicrobial Proteins
Components of innate immune system that are against microbes
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Interferons (IFN's)
Are cytokines - work agains the spread of any viral infection - Infected cells prevent the spread of the virus, by realizing IFN. - IFN bind to neighboring cell to prevent them from getting infected, stimulates NK cells and macrophages to destroy virus infected cells
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Complement System
``` Antimicrobial group of substances of innate immunity Serve to protect body against pathogens -Opsonization - Inflammation - Cytolysis - Elimination of immune complexes ```
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Classical Pathway
Complement proteins bind to an antibody that has previously attached to a foreign substance
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Alternative Pathway
Surface of polysaccharides of certain bacterial and fungal cell walls bind directly with a complement protein
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Complement Sysptem: | Opsonization
Protein (complement) binds to bacteria or other cell type (to be identified) so ti can be phagocitized.
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Complement System: | Inflammation
Complement increases inflammatory response by activation of mast cells and basophils and by attracting neutrophils and macrophages
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Complement System: | Cytolysis
Many complement components trigger direct killing. Form a protein channel plasma membrane of target cell MAC, (Membrane Attach Complex) causing the cell to lyse (a lot of fluid inside cell).
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Complement System: | Elimination of immune complexes
Complements bind antigen-antibody to erythrocytes to be transported to the liver and spleen. Where they are striped by macrophages, erythrocyte continue to circulate the blood
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Inflammation / Inflammatory Response
Nonspecific even that occurs in vascularized tissue against a variety of injury-causing stimuli.
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Events of Inflammation
1. Release of chemicals from injured cells, mast cells, basophils, and infectious organisms. Include: Histamine, prostaglandin, leukotrienes, chemotactic factors. 2. Chemicals trigger vascular changes: Increase capillary permeability and capillary endothelium to provide Cell-Adhesion Molecules (CAMs) 3. Leukocytes go to infected tissue by: a) Margination - leukocytes CAMs attach to capillary endothelium CAMs. b) Diapedesis is where cells squeeze out of the vessel wall cells c) Chemotaxis is migration of leukocytes along chemical gradient. They are attracted by the chemicals released from damage cells, dead, or invading pathogen (chemical gradient) 4. Plasma proteins go int injured area (immunoglobulins, complement, clotting proteins and kinins. -clotting proteins lead to formation of a clot that walls of microbes and prevents them from spreading into the blood and tissues -Kinins (bradykinin) increase capillary permeability and stimulate pain receptors (stimulus for causing pain associated with inflammation) 5. Exudate
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Exudate
Materials like: increase fluid, protein, and immune cells leave the capillaries and then enter the interstitial space of the tissue. Which delivers cells and substance needed to eliminate injurious agent and promote healing
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Cardinal Signs of Inflammation
1. Redness due to increase blood flow 2. Heat due to increase blood flow and increase metabolic rate with in the area 3. Swelling result from increase fluid loss from capillaries into the interstitial space 4. Pain due to accumulation of interstitial fluid, and chemical irritation by kinins, prostaglandins,and substance release from microbes. 5. Loss of function due to pain and swelling (more severe cases)
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Acute Inflammation Response
inflammatory response last no longer 8-10 days
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Chronic inflammation
Inflammation occurs for more than 2 weeks
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Fever (pyrexia)
Abnormal elevation of body temperature.
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Pyrogens
Interleukin 1, interferons, toxins produced by infections agents, response trauma, drug reaction or brain tumors.
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Events of Fever?
Pyrogens are release and circulate the blood, they target the hypothalamus and cause the release of prostaglandin E2. 1. Onset - Hypothalamus stimulates blood vessels in the dermis of the skin to vasoconstrictor to decrease heat loss. Person shrivers to increase heat production making body temp rise 2. Stadium - Elevated temperature is maintained. Metabolic rate increase to have more heat. Liver and spleen bind to zinc and iron (which are minerals needed for microbes) to slow microbial reproduction. 3. Defervenscence- temperature returns back to normal, the hypothalamus is no longer stimulated by pyrogens, prostaglandins release decreases. Hypothalamus stimulates vasodilatation of blood vessels and the skin and sweating to release heat
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Immune Response
Lymphocytes form and what they secret
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Cell-Mediated Immunity
Immune response involving T-lymphocytes
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Humoral Immunity
Immune response involving B-lymphocytes that develop into plasma cells to synthesize and release antibodies
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Antigen
substance that binds to a components of adaptive immunity
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Foreign Antigens
non-self antigen bind with in the body immune components, different than human body's molecules
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Self antigens
Body molecules, that do not bind to body immune components
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Autoimmune Disorder
own immune system reacting to self-antigens, as if they where foreeing
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Antigenic Determinant / Epitope
Specific site of the antigen molecule that is recognized by components of the immune system
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Immunogen
Antigen that induces an immune response
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Immunogenicity
Immunogen ability to cause an immune response
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Haptens
Too small to functions as an antigen alone, need to attach to a carrier molecule in the host, and become antigenic and trigger and immune response
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Receptor complex
T-lymphocytes and B-lymphocytes receptors, Different and separate proteins, about 100,00 receptor complexes per cell
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TCR (T-cell receptor)
antigen receptor (portion of a receptor complex) of T-lymphocytes
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BCR (B-cell receptor)
antigen receptor of B-lymphocytes
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Helper T-lymphocytes / CD4
Activate B-lymphocytes, contain CD4 proteins in the plasma membrane
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Cytotoxic T-lymphocytes / CD8 cells
Release chemicals that are toxic to cells, resulting in destruction, Contain CD8 plasma membrane protein
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Antigen Presentation
Presenting of antigen on plasma surfaces, so T-lymphocytes can see the antigen
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Antigen Presenting Cell
Communicate the presence of antigen to T-lymphocyes and B-lymphocytes
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Major Histocompatibility Complex
Specialized transmembrane protein where antigen is attached
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MHC class I molecule
Are glycoproteins on nucleated cells, where antigen attaches too.
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Synthesized of MHC I?
1. Synthesized by RER, peptide fragments bind to MHC class I molecules 2. They are transported in vesicles through he endomembrane system, through the Golgi apparatus to the plasma membrane. 3. Vesicle fuses to plasma membrane and MHC class I molecules and antigen or self antigen are displayed within the plasma membrane
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Major Histocompatibility II molecule
``` Found on antigen presenting cells -Dendritic cells, macrophages, B-lymphocytes (all display both MHC class I, and II) ```
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MHC class II Molecule Synthesize
1. MHC class II is synthesized in Rough Endo Plasmic Reticulum then its 2. Packed into vesicles and shipped to Golgi Apparatus 3. Exogenous antigen is phagositozed by the cell. A phagosome (vesicle) is formed, then meets with lysosome to form a phagolysosome. Substance is digested into fragments 4. Vesicles containing MHC II is combined with vesicles containing the antigen 5. MHC class II molecule and foreign antigen are displayed with in the plasma membrane Provides means of communication specially to Helper T-lymphocytes
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Organ Transplant
Transfer of an organ from one individual to another. Before transplant donor and recipient are tested for major histocompatibility Complex antigens and the ABO blood group antigens. Because MHC molecules can be detected by immune system as foreign and cause rejection.
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Exogenous Antigen
Pathogens, cellular debris, or other potential harmful substance located outside of cell, and are engulf by APC
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Activation of Helper T-lymphocytes: | First Response
- First Stimulation - Physical contact with APC and Helper T-lymphocyte. Antigen was engulf and is displaying on APC membrane surface with MHC class II molecule - TCR of T-lymphocytes bind to peptide fragment (antigen)presented with an MHC class I molecule of the APC. - Stabilizing CD4 molecules of the helper T-lymphocytes binding to other regions of the MHC class II molecule.
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Activation of T-Lymphocytes | Second Stimulation
- Helper T-lymphocytes begin to secrete cytokine Interleukin 2 (IL-2) occurs within 24 hrs. - T-lymphocytes poliferate to form a clone of helper T-lymphocytes (the cells produced are: helper T-lymphocytes that continue to produce IL2, and memory helper T-lymphocytes for subsequent encounter with the specific antigen
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Activation of Cytotoxic T-Lymphocytes | First Stimulation
- CD8 binds with MHC class I molecule of infected cell, TCR interacts with antigen within MHC class I molecule
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Activation of Cytotoxic T-lymphocytes | Second Stimulation
IL 2 of helper T-lymphocytes bind to cytotoxic T-lymphocytes, acts as a paracrine hormone to stimulate the cytotoxic T-lymphocytes
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Activation of B-Lymphocytes | First Stimulation
Antigen bind to BCR and antigen cross-links BCR's. B-lymphocytes engulfs, processes and presents antigen to helper T-lymphocytes that recognizes the antigen.
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Activation of B-lymphocytes | Second Stimulation
Activated helper T-lymphocyte releases IL4, to stimulate B-lymphocytes Activation of B-lymphocytes causes proliferation and differentiate into plasma cells that produce antibodies, and the remainder become memory B-lymphocytes that are activated upon reexposure of the same antigen
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Lymphocyte Recirculation
B and T-lymphocytes circulate through the blood and lymph every several days Provides delivery of different lymphocytes to secondary lymphatic structures, making it more likely that a lymphocyte will encounter its antigen, if present.
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Effector Response
Activate lymphocytes use to help eliminate the antigen
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Antibody Titer
Circulating blood concentration of antibody against a specific antigen
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Antibody Immunoglobulin
Tags the antigen, so it can be eliminated
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Antibody Monomer
4 polypeptide chains are held together by disulfide bonds
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Variable Regions
Antigen binding site, attaches to a specific antigen. Binds to antigen through weak intermolecular force, including hydrogen bonds, electrostatic interactions, van der Waal forces and hydrophobic interactions
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Constant Region
Contains FC region,, portion of the antibody that determines the biological functions of the antibody.
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Actions of Antibodies: | Neutralization
Antibody covers an antigenic determinant of a pathogen | Antibody attaches to pathogen binding cell receptor to prevent it from attaching to a cell
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Action of Antibodies: | Agglutination
Antibody cross-links antigens of foreign cells, causing them to clump
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Actions of Antibodies: | Percipitation
Antibody can cross-ling soluble, circulating antigen such as viral particles (not whole cells) to form an antigen-antibody complex. Wait fro phagocytic cells to be engulfed and eliminated
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Fc Region: | Complement Fixation
Fc region of some classes of antibodies can bind to complement protein
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Fc Region | Opsonization
Fc region of antibody binds to receptors of phagocytic cells triggering phagocytosis
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Fc Region | Activation of NK cells
Fc region of antibody binds to a NK cell, triggering the release of cytotoxic chemicals called ---Antibody-dependent cell-mediated cytotoxicity (ADCC)
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IgG
Major class of immunoglobulins Location: Body Fluids-->blood, lymph nodes cerebral spinal fluid, serous fluid, peritoneal fluid Function: Neutralization(virus, bacteria, toxins) - agglutination, precipitation, complement activation, opsonization, natural killer cell activation _Passive immunity crosses the placenta, component of breast milk "I Gave Good milk"
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IgM | Location, Function,
B-lymphocyte receptor, responsible for rejection blood transfusion Location: found in blood Action: Neutralization, agglutination, Complement binding