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Immunology > Chapter 2&3: Innate Immunity:Immediate Response To Infection/Induced Response To Infection > Flashcards

Chapter 2&3: Innate Immunity:Immediate Response To Infection/Induced Response To Infection Flashcards

1
Q

Mechanical and Chemical Barriers:

Skin

A
  • protects the deeper tissues of the body
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2
Q

Mechanical and Chemical Barriers:

Mucous Membranes

A
  • lines the epithelium of the digestive and respiratory tracts
  • prevents penetration of parasites into tissues
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3
Q

Mechanical and Chemical Barriers:

Gastric Juices

A
  • salivary glycoproteins, lysozyme, oleic acid on the skin, ures
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4
Q

Mechanical and Chemical Barriers:

Acidity

A
  • stomach and vagina

- kills unwanted bacteria and yeast

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5
Q

Mechanical and Chemical Barriers:

Bile

A
  • aids in fat digestion

- inhibitory substance against parasites

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6
Q

Mechanical and Chemical Barriers:
Antimicrobial Peptides
Cationic Antimicrobial Peptides

A
  • damage bacterial plasma membranes through electrostatic interaction
  • positively charged peptides that bind to the bacteria cell wall (defensins drills a hole)
  • makes the content leak out of bacterial cell
    Examples:
    Cathelicidin
    Defensins
    Histatins
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7
Q

Mechanical and Chemical Barriers:
Antimicrobial Peptides
Bacteriocins

A
  • plasmid-encoded antibacterial peptides produced by normal bacterial flora
  • lethal to related species through a variety of mechanisms
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8
Q

Mechanical and Chemical Barriers:

Lysozyme

A
  • chemical inhibitor of a nonspecific nature
  • found in human tears, seat, and saliva
  • disrupts the cell walls of gram-positive by digesting peptidoglycan
  • catalyzes the hydrolysis of 1,4-beta-linkages between N-acetylmuramic acid (NAM) and N-acetyl-D-glucosamine (NAG) residues in a peptidoglycan (found in the cell wall of bacteria)
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9
Q

Mechanical and Chemical Barriers:

Interferons

A
  • groups of substances produced by body cells in response to invasion by viruses
  • interferons trigger the production of inhibitory substances that interferes with viral reproduction
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10
Q

Complement

A
  • set of 20 serum proteins that enhance phagocytosis through inflammation, opsonize pathogens for phagocytosis, and lyse cells through the formation of membrane attack complex (MAC)
  • MACs form large hole in the membranes of many microorganism, especially gram negative bacteria and enveloped viruses
  • small peptides released during complement activation induce local inflammation
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11
Q

Three Pathways of Complement Activation:

1. Alternative Complement Pathway

A
  • occurs in response to intravascular invasion by bacteria and some fungi
  • involves interaction of complement with the surface of the pathogen forming the membrane attack complex
  • at the start of an infection, complement activation proceeds by the alternative pathway
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12
Q

Three Pathways of Complement Activation:

Lectin Complement Pathway

A
  • also called Mannan-Binding Lectin Pathway
  • occurs when macrophages stimulate liver cells to release acute phase proteins such as mannose-binding protein (a lectin), which then can activate complement via the alternative pathway or the classical pathway
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13
Q

Three Pathways of Complement Activation:

Classical Pathway

A
  • results from antigen-antibody interaction that occur during specific immune responses
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14
Q

C3 Convertase

A
  • all complement pathways activate this to lead to different outcomes
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15
Q

C3 convertase to C3a,C35a

A
  • peptide mediators of inflammation phagocytose recruitment
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16
Q

C3 convertase to C3b

A
  • binds to complement receptors on phagocytes

- opsonization (small proteins that coat microbes as a signal for a bug) of pathogens

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17
Q 
C3b to Terminal complement components:
C5b
C6
C7
C8
C9
A
  • C5b6789 membrane attack complex, lysis of certain pathogens and cells
18
Q

Complement Receptor (CR1) on Macrophages

A
  • detects C3b coated on bacteria

- macrophages then engulf the C3b bacteria complex

19
Q

Membrane Attack Complex

A
  • causes cell lysis

- the terminal complement proteins lyse pathogens by forming a membrane pore

20
Q

Why doesn’t our complement destroy our cells?

A

Two Possible Reasons

  • our body produces CD59 which prevents the MAC formation from disallowing C9 from fusing
  • complement is also in inactivated state when we have no infection
21
Q

Moderate Fever Benefits Hosts Defenses

A
  • low to moderate fever supports the immune system by inhibiting rapid microbial growth, encouraging rapid tissue repair, and heightening phagocytosis.
  • most common cause of fever is viral or bacterial infection, usually due to action of an endogenous pyrogens and inflammatory cytokines (IL-1, IL-6, and TNF)
22
Q

Natural Killer Cells

A
  • recognize and kills abnormal cells
  • are defensive lymphocytes that act spontaneously on virus (infected cells, cancer cells, or organ transplants)
  • when an NK recognizes a cell as “nonself” it releases cytotoxic perforins and granzymes
  • produce receptors that seeks abnormal things on cells
  • main circulatory lymphocytes that contribute to the innate immune response
  • activated by interfurons (signals proliferation of NK cells)
23
Q

NK Cells Recognizes and Target in 3 Ways

A
  1. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
    - receptors on NK cells link them to antibody-coated target cells
  2. If NK cells bind class 1 Major Histocompatability (MHC) molecule
    - if MHC is on cell, killing is inhibited
    - no MHC Class 1, then killing occurs through pore-forming proteins and cytotoxic enzymes (granzymes)
  3. Production of MIC Ligand
    - if MIC Ligand is produced by infected cell, it automatically signals perforins and granzymes that tells NK that it is abnormal
24
Q

Pyrogenic Cytokines

A
  • inflammatory cytokines raise body temp and activate the liver to make the acute-phase response
25
Q

Phagocytosis

A
  • represents part of a second line of nonspecific defense and a first line of cellular defense against invading microorganisms
  • are monocytes, tissue macrophages, dendritic cells, and neutrophils
  • process by which invaders are recognized, ingested, and killed
26
Q

Process of Phagocytosis

A
  • begins with invagination of the cell membrane to form vesicle
  • vesicle pinches off and fuses with several lysosome (organelles that contribute digestive enzymes, proteins and peptides to the digestion process
27
Q

Chemotaxis

A
  • binding of bacteria to macrophages and neutrophils induces chemokines that attract other macrophages and neutrophils to the area
28
Q

Opsonins

A
  • attach to microbes to increase the ability of phagocytes to adhere (opsonization)
29
Q

Exocytosis

A
  • the antigenic remains of invaders can be expelled from the cell (as neutrophils do) or further processed for antigen presentation on the lymphocyte cell surface (as macrophages and dendritic cells do)
30
Q

Phagosome

A
  • phagocytized microbes are held in a phagosome
  • is acidified, killing or inactivating the pathogen
  • also fuse with lysosome (phagolysosome)
  • enzymes and other products kill and digest the pathogen
31
Q

Tissue Macrophage

A
  • carry a battery of phagocytic and signaling receptors
32
Q

Pathogen-Associated Molecular Patterns (PAMP)

A
  • help the innate immune system recognize pathogens
    Examples:
    Lipopolysaccharide (LPS) on bacteria
33
Q

Toll-like Receptors (TLRs)

A
  • signaling receptors on:
    Macrophages
    Dendritic Cells
    Endothelial Cells
  • sense the presence of infection
  • TLRs mediate a specific response to distinct PAMPs
  • stimulate the secretion of cytokines
    Example:
    Those that stimulate production of acute phase protein
  • the TLRs response must be regulated to prevent infection and immune disorders
34
Q

Innate Immune Receptors Distinguish Features of Microbial Structure

A
  • Innate Immunity depends on Receptor Recognition of Common Pathogen-Associated Molecules
35
Q

Inflammation

A
  • nonspecific defensive response by the body to an injury in the tissue
  • develops after mechanical injury (blow to skin) or to a chemical agent (acid or bee sting)
  • activation of resident macrophages induces inflammation at sites of infection
  • response can also be due to an infection by a living organism, like a parasite
36
Q

Process of Inflammation

A
  • tissue injury or paraste infection triggers the release of chemical mediators (histamines), which triggers vasodilation, and increase capillary permeability at the site of infection
  • macrophages and neutrophils march in to clear parasite
  • inflammatory cytokines recruit neutrophils from the blood to the infected tissue
  • homing of neutrophils to inflamed tissues involves altered interactions with vascular endothelium
  • neutrophils are potent killers of pathogens and are themselves programmed to die
  • pus is a product of phagocytosis during inflammation
  • when pus becomes enclosed in, a wall of fibrin forma a sac, this sac is an abscess or boil
37
Q

Four Characteristic Signs of Inflammation

A

Rubor: redness from blood accumulation
Calor: heat from the warmth of the blood
Tumor: swelling from the accumulation of fluid
Dolor: pain from injury to local nerves

38
Q

Numerous Inflammatory Mediators Function in Response

A
  1. Kallikrein
    - an enzyme that catalyzes formation of bradykinin
  2. Bradykinin
    - binds to capillary walls, causing movement of fluid and leukocytes into tissue and production of prostaglandins (cause pain)
    - bind mast cells, causing release of histamine and other inflammation mediators
    - Histamine- promotes movement of more fluid, leukocytes, bradykinin, and kallikrein into tissue
39
Q

Cytokines

A
  • released by macrophages upon activation
40
Q

Type 1 Interferons

A
  • inhibit viral replication and activate host defenses
  • group of substances produced by body cells in response to invasion by viruses
  • trigger the production of inhibitory substances that interferes with viral reproduction
  • internal detection of viral infection induces cells to make an interferon response
41
Q

Plasmacytoid

A
  • dendritic cells that are factories for making large quantities of type 1 interferons
42
Q

What happens when innate immunity fails?

A
  • NK cells and macrophages activate each other at sites of infection
  • if macrophage detects a virus, it will spit out cytokine produce IL12, which activates NK cells
  • interact w/ macrophage in induce apoptosis if macrophage can’t save infection
  • NK will also induce signals to help macrophage do its job better (Interfuron gamma)
    IF THIS CAN”T OCCUR
  • interactions between dendritic cells and NK cells influence the immune response
  • when NK cells are scarce and are outnumbered by dendritic cells, they drive the dendritic cells to mature into the form that initiates adaptive immunity (production of antibody B cell and T cells)

Immunology (13 decks)

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