Chapter 21 Immune System Flashcards

1
Q

Immune System

A

Provides resistance to disease

  • Composed of two intrinsic defense systems
  • Innate (nonspecific) defense system
    • constituites first and second line of defense
    • First line) Esternal body membranes (skin and mucosae)
    • Second line) Antimicrobbial proteins, phagocytes, and other cells. (Inhibut spread of invaders, activates inflammation)
  • Adaptive (specific defense system)
    • Third line of Defesnse) Attacks particular foreign substances.
  • Is a functional system rather than an organ system.
  • Inntate and adaptive defenses are interertined
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2
Q

Innate Defenses (Physical)

A

First/Second line of defense

  • Surface barriers) skin and mucous membranes along with secretions
    • Physical barrier reienforced with keritin to resist weak acids and bases as well as most microorganisms.
    • Mucoseae provide similar protection
  • Protective chemicals
    • Acid) skin acidity creates acid mantle which inhibits growth
    • Enzymes) Lyszysome of sliva, respritory mucus, lacrimal fluid, and enzymes in stomach kill many microorganisms
    • Mucin) sticky mucas that lines digestive and respritory tract and traps mircoorganisms.
    • Defensins) Antimicrobial peptides that inhibit growth
    • Other chemicals) Lipids in Sebum and Dermicidin in Sweat are tocix to bacteria
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3
Q

Internal Defenses (Second Line)

A

If microoganisms invade deeper tissues Phagocytes, Natural Killer (NK) cells, The Inflammatory response (Macrophages, mast cells, WBC’s and inflamatory chemicals) antimicrobial protiens, and Fever will trigger

  • Many second-line defense cells have pattern recoginition receptors that can reconize and disarm microbes before they cause harm
  • One class, Toll-Like Receptors (TLR’s) play a central role in triggering human immine responses
    • Humans have 11 diffrent TLR’s that each reconize a particular microbe.
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4
Q

Phagocytes

A

White Blood Cells (WBC’s) that ingest and digest foreign invaders

  • Neutrophils) Most abundent type of WBC.
    • become phagocytic to infectious materials
  • Macrophages (Big eaters)
    • derive from monocytes that leave blood stream aand enter tissues
    • Most Robust (cheif) phagocytic cell
    • Free macrophages) wander through tissue space (blood vessels)
    • Fixed macrophages) pernenent residents of organs (liver, brain)
  • Phagocytosis) Destruction of Forgien particles
  1. Phagocyte reconizes and adheres to pathogen’s carbohydrate “signature”
    • Opsoniztion) immune system antibodies/ protiens add opsonis that coat pathogens. Act as handles for phagocytes to grab on to
    • Some microorganisms have capsules that hide carbohydrates helping them evade phagocytosis.
  2. Cytoplasmic extension (psudopods) bind to particle and engulf into a vessicle called a Phagosome
  3. Phagosome fuses with lysosome > Phagolysosome
  4. Phagolysosome is acidified. Lysosomal enzymes digest particles
  5. Indigestible waste is exocytosed from the phagosome.
  • Cells immine to phagocytosis are helped by T cells via
    • The release of cell-killing free radicles
    • Production of oxidizing chemicals (H2O2)
    • Increase of pH and osmolarity of phagolysosome
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5
Q

Natural Killer (NK) Cells

A

Nonphagocytic, Large Granular Lymphocytes that police blood and lymph

  • Can kill cancer and virus-infected cells before adaptive immune system is activated.
  • Attack cells that lack cell-suface recsptors calles MCH (major histcompatibility complex)
  • Kill by inducin apoptosis (programed cell deth) in cancer cells and virus-infected cells.
    • secrete chemicals that enhance inflammatory response.
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6
Q

Inflammation

A

Triggerd whenever bodytissues are injured.

  • Benifits of inflmation
    • Prevents spread of damaging agents
    • Disposes of pathogens
    • Alerts adaptive immune system
    • Sets the stage for repair
  • Four Signs of acute infmation
    • Redness, Heat, Swelling, Pain (somtimes function is impared)
  • Stages of inflmmation
    • Inflammatory chemical release
      • released into ECF
      • Major is histamine, Other inflammatory chemicals include Kinins, prostaglidins (PG’s) cytokines and complements if inflmation is caused by pathogens.
      • All chemicals casue vasiodlation of local arteris, leaky capillaries, and attract phagocytes.
    • Vasodilation and Increased Vascular Permiblity
      • Hypermia) increased blood flow in response to vasodilation.
      • Exudate) Antibodies leak into tissue due to increased permiability
      • Edema) Delivers clotting protiens in a surge of fluid from lymph vessels. Clotting factors form structure for repair.
    • Phagocyte Mobilization
      1. Leukocytosis) Release of nutrophils in response to lukeocytosis-inducing factors
      2. Migration) cell adehsion factors (CAM’s) from inflamed area signal cells to moce into place
      3. Diapedesis) neutrophils flatten and squeeze between endothelial cells to inflamed area
      4. Chemotaxis) Inflamatory chemical signal nutrophils to start chemotaxis to remove foreign debris.
      • Nutrophils lead; macrophages follow
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7
Q

Pus/ Abscess

A
  • Pus) Creamy yellow mixture of dead neutrophils, tissue/cells, and living/dead pathogens
    • An abcess forms when inflammatory mechanism fails to clear the debris from the area. The sac of puss is walled off and may need to be drained surgically to drain
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8
Q

Antimicrobial Proteins

A
  • Ehance innate defense by
    • Attacking miroorganims directily
    • Hindering microorganims abilty to reproduce
  • Most important antimicrobial protiens
  • Interferons (INFs)
    • warn helthy neighboring cells and stimulate production of protiens that block viral reproduction
    • degrade viral DNA
    • IFN α and β protiens) activate NK cells
    • IFN γ protiens) Activate macrophages
  • Complement System
    • at least 20 plasma protiens that circulate in incactive form. Included protiens C1-C9 and factors B, D, and P
    • Major mechanism for destroying forgein substances and enhances inflammation
    • Ehnances both innate and adaptive defenses
  • Complement Activation
    • Classical Pathway) Abtibodies bind to compelment protiens
    • Lectin Pathay) Lectins are protiens molcecules that activate complement protiens
    • Alternative Pathway) C3 is spontaneously activated and activates compliment protiens.
  • Cell lysis begins when C3 splits its C3b componat binds to the target cell. This triggers the Membrane Attack Complec (MAC)
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9
Q

Fever

A

Abnormally high body temp that is systemic response to invading microorganims

  • Lukeocytes and macropgages release pyrogens
    • Pyrogens act on body’s themostat in hypothalamus which raises the body them
    • Causes liver/ spleen to hold iron and zinc which slows bacterial growth
    • Increase metabolic rate which increases rate of repair.
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10
Q

Adaptive Defenses

A

Adaptive immine system is a specific defensive system that eliminated almost any pathogen or abnormal cell in the body.

  • Activies
    • Amplifies inflammatory response
    • Activates complement
    • Must be primed by inital exposure to specific forgein substance which takes time.
  • Charcteristics of Adaptive immunity
    • Specific) Targets specific antigens
    • Systemic) Not restriceted to inital site
    • Memory) Remembers and mounts srtonger attacks when enountering an antigen for a subsequent time
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11
Q

Two branches of adative immune system

A
  • Humoral (anitbody-mediated) immunuty
    • Antibodies produced by lympocytes circulate freely
    • Bind to target cell to temoporally inactive and mark them for destruction by phagocytes or compliment,
  • Cellular (cell-mediated) immunity
    • Lympcytes act directily against target cells
    • Directily) Killing infected cells
    • Indirecityly) Releasing chemicals that increase inflammatory response or activate other lymphocytes or macrophages
      *
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12
Q

Antigens

A

Substances that can mobilize adaptive defenses and provoke and immune response.

  • Targets of all adaptice immine response
  • Large, complex moleculea not normally found in the body
  • charcteristice of antigens
    • can be complete or hapten (incomplete)
    • Conatain antigentic deterninants
    • can be a self-antigen
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13
Q

Complete Antigens or Haptens

A
  • Complete antigens) have two functional properties
    • Immunogenicity) ability to stimulate proliferation of speciifc lymocytes
    • Reactivity) ability to react with activated lympocytes and antibodies
  • Incomplete antigens also called haptens
    • moleculeas are too small to be seen and not immnogenic by themselvles.
    • The combination of a hapten and protein is seen as a forgein invader by the body.
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14
Q

Antigenic Detrminants

A
  • Parts of anigen that antibodies or lympocyte receptors bind to
    • Mobilize several diffrent lympocyte populations; Form different kinds of antibodies agaisnt them
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15
Q

Self-Antigens (MHC proteins)

A
  • Self-Antigens) all cells that are covered with a veriety of proteins located on the suface that are not anitgenic to ones self but could be antigenic to others.
    • occurs during transfusions or graphs
    • Major Histocompatibity Complex (MHC) are unique to each indvuidal
    • T lymphocytes can reconize only antigens that are presented on MHC proteins
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16
Q

Cells of Adaptive Immune System

A
  • Two types of lymphocytes
    • B lymphocytes (B cells) - humoral imminity
    • T lymohocytes (T cells) - Cellular immunity
  • Antigen-presenting cells (APC’s)
    • Do not respond to specific antigens
    • Play essential auxiliary roles in immunity. For example, T cells can only bind antigens that are presented.
17
Q

5 Stages of Lympohocyte Development, Maturation, and Activation

A
  1. Origin)
    • Both orginate in red bone marrrow
    • Share common pattern of devlopment in life cycles
  2. Maturation
    • “educated” in a 2-3 day process. mature in primary lymphoid organs (B cells in bone marrow, T cells in thymus)
    • Immunocometence) lympcytes must be able to reconize correct antigen
    • Self-Tolerance) lympocytes must not attach their own antigens
  3. Seeding secondary lymphoid organs and circulation
    • Immunocometent B/T cells are naive when not exposed
    • Movment to a secondary lymphoid orggan (lymph nodes, spleen) increases chance of enounter with antigen
  4. Antigen enounter and activation
    • First enounter with an antigen triggers lymphocyte to develop further
    • Lymphocyte differentiates into active cell by binding to a specific antigen. (clonal selection)
  5. Proliferation and differntation
    • Once selected and activate, lymphocute proliferates
    • forms an army of clones
    • Effector cells) fight infections
    • Memory Cells) store information about anitgen
18
Q

Antigen Receptor Diversity

A
  • Genes, not antigens, detemine which foreign substances the immune system will reconize
  • Lympocyte education during maturation
    • Positive Slection) selects T cells capabile of reconizing self-MHC proteins tnat can’t be festroyed by apoptosis. Makes strong immune cells.
    • Negative Selwevtion) Prompts apoptosis of T cells that bind to self-antigens. Makes sure immune cells do not attack the body
19
Q

Antigen-Presenting Cells

A
  • Engulf antigens, break them apart, and present fragments to T cells for recognition.
  • Major types
  • Dendritic cells)
    • Found in skin. Phagotize patogens that enter tissue than present antigens to T cell in lymph node
    • Most effective antigen presenter
    • Key link between adaptive and innate immunity
  • Macropages)
    • Found distrubuited in CT and Lymphoid organs. Present antigens to T cells and activates more macrophages
    • Become phagocytic killer cells to kill infection. Also activate inflammatory responses
  • B Lymphocytes
    • Do not activate T cells. Present antigens to helper T cells to obtain “help” with own activation
20
Q

Humoral Immune Response

A
  • When B cells enounter an antigen it triggers the humoral immune response
    • Antibodies are produced for specific antigen when antigen activates B cell surface receptors
    • This leads to the proliferation of more B-cells (clone cells) with the same antibody secreting ability known as plasma cells
  • Plasma cells secrete antibodies at a rate of 2000 molecules per seocond for 4-5 days then die
    • Antibodies circulate blood and lymph and bind to free antigens to mark them for destruction by innate or adaptive immune defenses.
  • Clone cells that do not become B cells become meory cells which store information abou the immune response for future use.
21
Q

Immunological Memory

A
  • Primary immune response
    • Body is esposed to anitgen for the first time. There is a lag period of 3-6 days before immune response is mounted
    • Peak antibody levels are 10 days after exposure
    • Antibody levels then decline
  • Secondary Immune Response
    • Re-eposure to same antigen is a faster repsonse because of memory cells’ immunological memory
    • respond within hours not days. Peak antibody levels 2-3 days after
    • Antibodies are stronger and can remain high for weeks/months.
22
Q

Active Humoral Immunitu

A
  • Occurs when B cells enounter antigens and produce specific antibodies against them
    • Naturally aquired) formed in response to actual bateria/ virus
    • Artifically acquired) formed in response to vaccine of dead or attenuated pathogens.
      • Spare us of primary reposnse symtoms.
23
Q

Passive Humoral Immunity

A
24
Q

Antibodies

A
  • Antibodies (Immunoglobuline (IBGs) are proteins secreted by plasma cells
    • made of gamma globulin
    • Capabule of binding specifically with antigen dtected by B cells
  • Basic Structure
    • T or Y shaped
    • Four looping polypetide chains linked by disulfide bonds
      • Two identical heavy (H) chains and two light (L) chains
      • Variable (V) regions at one end of each arm
  • Antibody Classes
    • IgM, IgA, IgD, IgD, IgE
  • Functions
    • Inactivate and Tag antigens
    • Forms antigen-antibody (Immune) complexes
25
Q

Defensive Functions of Antigens

A
  • Nutralization)
    • Block specific sites on antigen so it is innate
  • Aggulitnation
    • Clumps antigens into large clumps to be destroyed because each antigen has more than one active site.
  • Precipitation
    • Makes easier for phagocytes to engulf
  • Complement Activation
    • Several antibodies bound close togehther on the same cell can cause the cell to lyse (burst)
    • Also can amplify other functions (immune response)
26
Q

Cellular Immune Response

A
  • T cells defend against intracellular antigens
    • Some directly kill cells, some release chemicals that regulate immune response
  • Two major Populations of T cells
    • CD4 cells) usually become Helper T Cells (TH) that can activate other B cells
      • some become regulatory cells and some become memory T cells
    • CD8 cells) become cytotoxic T cells (TC) capable of destroying cells with forgein antigens
      • can also become Memory T cells
  • Helper, Cytotoxic, and Regulatory T cells are activated T cells
  • Naive T cells are CD4 or CD8
27
Q

Activation of T cells

A

Activated when an Antigen is prsented to them. Two Steps

  • Antigen Binding
    • T cell antigen receptors (TCR’s) bind to antigen-MHC complex on APC surface
    • TCR reconizes both self-antigens (MHC) and froeign antigens
    • Signals T cell to activate
  • Co-stimimulation)
    • T cell must bind to co-stimilatory signal on surface of APC to divide and secrte cytokines
28
Q

Proliferation and Differentiation of T cells

A
  • T cells enlarge and proliferate in response to cytokines
    • Cytokines) chemical messangeres of immune system that mediate how cells develop and respond
  • Differentiate and preform functions according to T cell class.
  • T cell respone time
    • Primary response peaks within a week
    • After 7-30 days T cell death (apoptosis) begins
      • Hazardous if not because of the inflammatory cytokines released by T cells
29
Q

Helper T (TH) cells

A
  • Central role in Adaptive Immune Response) Activate humoral and celluler arms
    • Activate B cells and other T cells
    • Induce B and T cell proliferation
    • Secrete Cytokines that recruit other immune cells
  • Without TH there is no immune respnonse
  • Activation of B cells
    • TH cells diretly intract with B cells displaying antigen fragments bound to MHC receptors
    • B cells may be activated without TH cells by binding to T cell-independent antigens.
30
Q
A
31
Q

Cytotoxic T (Tc) cells

A
  • Directly attack and kill other cells
  • Circulate in blood and lymph and search for any anitgens they reconize
    • Virus-Infected cells
    • Cells with intracellular bacteria/ parasites
    • Cancer cells
    • Foreign cells
  • Can kill cells via one of two mechanisms
    1. Tc releases perforins (create cell pores for granzymes) and granzymes (stimulate apoptosis/ cell death)
    2. Tc cell binds to specific membrane receptor on target cell and stimulates apoptosis.
32
Q

Organ Transplants/ Rejection

A
  • Allograft) organ tranplant from same species
  • Sucess depends on
    • ABO and other blood antigens
    • MHC antigens are matched as closley as possible
  • After surgery
    • Pateinet is treated with immunosupresive therapy to prevent immune system from overacting
    • Immune system cannot protect body from foreign agents
    • Best Circumstances: organ rejection is ten years after surgury
33
Q

Immunodefiency

A
  • Condtions that impair fucntion or pruduction of immune cells/ molecules
    • Severe Combined Immunodefiency (SCID) syndrome) Marked with a deficit in B and T cells
      • Treatment is bone marrow transplants
34
Q

Acquired Immune Defiency Syndrome (AIDS)

A
  • Human immunodefiency virus (HIV) cripples immune system by interfering and destryoying TH Cells.
    • Chacterixed by weight loss, night sweats, and swollen lymph nodes
    • Transmited via body fluids
  • Leads to development of AIDS symptome
    • No cure, but four classes of anitvirals can help
35
Q

Autoimmune Diesease

A
  • Immune system loses abiluty to distinguish self from foreign
    • Autoimmunity) Production of autoanibodies and senative TC cells that destroy body tissue
  • Examples
    • Rhumatoid Arthritis) Destroys Joints
    • Multiple Sclerosis) Destroys White Matter myelin
    • Graves’ Disease) causes hyperthyroidism (thryoid)
    • Type 1 Diabetes) destroys pancratic cells
  • Treatment
    • Suppress entire immune system
36
Q

Hypersenitivity

A
  • Immune system damages tissues as it fights a precived threat that is in relality harmless
  • Distinguised by their time course and weather T cells or anitbodies are involved
    • Antibodies cause immediate and subacute hypersensitivities
    • T cells cause delayed hypersenitivy
  • Immediate Hypersenitivity
    • Begins in seconds after contact with allergen (antigen that causes reaction)
    • Inital reaction sensatizes us to allergen, subsequent reactions causes histamene release and induced inflammation.
    • Hitamenes causes runny nose, itchy hives, or watery eyes (all local responses).
    • Systemetic respons is anaphyletic shock (bronchiles constrict, vasodilation)
      • Tratment epineprine.
37
Q

Developmental Aspects of Immune system

A
  • Influences on Immune system function
    • Nervous system: depression, emotional stress, and
      grief impair immune response
    • Diet: vitamin D is required for activation of CD8
      cells > TC cells
  • With age, immune system begins to wane.