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Pathophysiology > Immune System > Flashcards

Immune System Flashcards

1
Q

Koch’s four postulates

A
  1. Pathogen must be found in every host and every case
    2.Same pathogen must be isolated from host and grown in pure culture
  2. when placed in a healthy host, that pathogen must cause the same disease
  3. When pathogen is isolated from the new host, it has to be proven the original pathogen
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2
Q

Antibiotics

A

Chemical substances derived from mold or bacteria that kill micro-organisms

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3
Q

Immunity

A

ability of the body to resist or eliminate potentially harmful foreign materials

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4
Q

Immune System Functions

A
  1. Defends against invading pathogens
  2. Removing worn out cells
  3. Identifying and destroying abnormal cells
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5
Q

Immune responses turned against healthy host cells lead to

A
  1. Auto-immune disorders
  2. Allergies
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6
Q

Monocytes

A

Transformed into macrophages; tissue-bound, and phagocytic specialists

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7
Q

Primary pathogens that activate the immune system

A
  1. Bacteria -
  2. Viruses ( more common - 94% of febrile illness - acellular
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8
Q

Lymphocytes

A

(especially in the lymphatic system)

  1. B lymphocytes - turn into plasma cells that secrete antibodies
  2. T lymphocytes - cell mediated immunity (from Thymus)
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9
Q

Leukocytes

A

Immune system effectors.
(arise from bone marrow)

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10
Q

Neutrofils

A

highly mobile phagocytes

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11
Q

Eosinopohils

A

Secrete chemicals to fight parasites; also involved in allergic reactions

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12
Q

Basophils

A

Similar to mast cells. Release histamine and heparin, also involved in allergic reactions.

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13
Q

lymphoid tissue(s)

A

[store, produce and process lymphocytes]

  1. Bone Marrow (makes B lymphocytes)
  2. Lymph nodes
  3. Spleen
  4. Tonsils
  5. Adenoids
  6. Appendix
  7. Peyer’s patches in digestive tract
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14
Q

Innate (Non-specific) Immunity

A
  1. First line of defense
  2. Cannot recognize a specific pathogen - Binds to pathogenic markers
  3. Rapid but limited - works immediately when the body is exposed to a threatening agent.
  4. Non- selectively defends body from foreign invaders
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15
Q

Four innate immunity defenses

A
  1. Interferon
  2. Natural Killer Cells
  3. Complement System
  4. Inflammation
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16
Q

Adaptive Immunity

A

Specifically targets foreign material to which the body has already been exposed.

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17
Q

Inflammatory responses

A
  1. Resident macrophages defend against invasive bacteria in the first hour
  2. Redness: Arterioles serving the invaded area dilate
  3. Swelling: Histamine is released to increase capillary permeability in the area.
  4. Interstitial clots wall off inflamed area
  5. Plasma proteins can leave the blood and enter the area
  6. Pus: Neutrofils or monocytes emigrate from the blood into the area and destroy bacteria.
  7. Heat: Increased local metabolism
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18
Q

Opsonins

A

mark bacteria for destruction via macrophages and neutrofils

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19
Q

Drugs that suppress the inflammatory process

A
  1. NSAIDs
  2. Glucocorticoids
  3. Inflixmabe (Remicade)
  4. Chemotherapy drugs (methotrexate)
  5. Interferon transiently inhibits virus replication.
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20
Q

Interferon mechanisms

A
  1. Triggers the production of virus-blocking enzymes by potential host cells
  2. The enzymes remain inactive unless cells are attacked by viruses
  3. released nonspecifically from any cell infected by a virus.
  4. It has anticancer effects
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21
Q

Natural Killer Cells

A

(Effector Lymphocytes-naturally occuring)

Destroy virus infected and cancer cells by lysing membranes.
Immediate non-specific defense

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22
Q

Complement System

A

(Plays a role in adaptive immunity in addition)

  1. Made up of plasma proteins of the liver.
  2. Activated by exposure to particular carbohydrate chains on the surface of microbes and anitbodies produced by foreign invaders.
  3. Leads to the membrane lysing.

Has three paths:
(1) - Classical pathway - Ab - Ag binding - attracts immune system for destruction.
(2) - Alternate - microbe has PAMP - (peptidoglycan like) - circulating microbes bind directly
(3) - Lectin pathway - microbe has carbohydrate containing manmose on cell surface. Lectin - binds surgars only found on microbes.

**All pathways lead to C3 protein hydrolysis.
C3a + C3b —-> C3b leads to C protein activation
C9 - causes pore to form on microbe cell membrane that leads to cytolysis of dangerous cell.

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23
Q

Adaptive Immunity attributes and types

A

Specifically targets the foreign material to which the body has already been exposed.

  1. Antibody mediated (humoral response)
  2. Cell - mediated immunity
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24
Q

Immunity branches and elements

A

Innate and Adaptive

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25
Q

B-Cell Function

A
  1. Formed in the bone marrow and control antibody mediated immunity.
  2. Each B cell has a receptor for one type of antigen.
  3. Binding of B cell + antigen - creates B cell differentiation
  4. B cells proliferate plasma cells to secrete a specific antibody response to initial antigen.
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26
Q

Thymosin

A

Hormone secreted from the thymus to stimulate T cell production

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27
Q

Membrane Attack Complexes

A
  1. Antibody molecules attach to antigens on pathogen membrane.
  2. Complement proteins link two antibodies.
  3. Activated complement proteins attach pathogens membrane forming a membrane attack complex.
  4. MAC pore(s) lyse cell.
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28
Q

Lymphocyte attributes

A
  1. Lymphocytes have receptors to recognize one distinct antigen.
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29
Q

Toll-like receptors

A

(TLRs) are part of innate effectors that recognize generic traits of all pathogens. Begin defense immediately by producing cytokines.

Bridge between innate and adaptive.

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30
Q

IgG

A

Most abundant antibody. The only antibody that can cross the placenta conferring passive immunity to the fetus from mother. (Can also pass via breast milk)

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31
Q

IgM

A

Act as B-cell surface receptors for antigen attachment. 1st antibody form in infection. Fights antigens in blood, and functions in classical complement pathway.

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32
Q

IgA

A

Major antibody found in mucosa. Lines digestive, respiratory, and GI systems. Is passed passively mother to baby via breast milk.

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33
Q

IgE

A

Mostly involved with allergic rxns and parasitic worms. Aids in histamine release.

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34
Q

IgD

A

Uncertain function, found on B cell surfaces- may play a role in B cell maturation and maintenance.

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35
Q

Immune complex disease

A

Over eager Ab-Ag response causes damage to normal and invading foreign cells.

Can cause kidney damage.

Can occur in bacterial, viral or parasitic infections

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36
Q

Antibody anatomy

A

All antibodies are made up of five, interlinked peptide chains.

The binding sites on the y section determines its specificity

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37
Q

How antibodies coordinate with innate immunity

A

Amplify innate immune responses to promote antigen destruction.

Activate the complementary system and MAC.

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38
Q

Overactive complement system effects

A

Can damage the kidneys, joints, skin, and brain (MS theory)

39
Q

Primary response and secondary response (and what b cells do)

A

The primary response is delayed as it is learning a new antigen the antibodies respond.

B memory cells remain dormant and upon subsequent exposure to the same antigen the secondary response is more rapid, potent and longer lasting.

40
Q

Active vs. Passive immunity

A
  1. Active is from direct exposure to an antigen.
  2. Passive immunity is from the transfer of preformed antibodies (mother’s breast milk, vaccine)
41
Q

The antibody types present in blood types.

A
  1. Type A - B
  2. Type B - A
  3. Type O - none
  4. Type AB - both A and B
42
Q

Lymphocytes

A

Pluripotent stem cell of both B and T cells.

B and T cells populate the lymph nodes, spleen, and organs of the lymphatic system.

43
Q

Major histocompatibility complex (MHC) function

A

binds to peptide fragments from pathogens and displays them on cell surface for recognition and immune response by T-cells.

44
Q

MHC I location

A

Found on all nucleated cells (including platelets)

45
Q

MHC II location

A

On professional antigen presenting cells (APCs) like macrophages, B cells and activated T cells.

46
Q

Erythroblastosis Fetalis

A

Hemolytic disease from newborn if subsequent children have a different Rh factor than the mother.

47
Q

Epitopes

A

Surface feature of a 3 dimensional antigen that stimulates an immune response.

48
Q

Methods Antibodies use in inactivating pathogens?

A
  1. Neutralization
    Ab blocks viral binding sites; coats or opsonizes.
  2. Agglutination
    Ab combine with epitopes or antigen cell surfaces restricting their movement. Some Abs can bind multiple antigens simultaneously.
  3. Precipitation
    Ab combines with dissolved antigens to form lattice-like arrangements that removes antigens.
  4. Complement System
    Leads to an attack on the cell membrane that kill the antigen.
49
Q

Types of Antibody categories.

A
  1. Polyclonal - naturally made in the body. Has affinity for one antigen but multiple epitopes.
  2. Monoclonal - binds to only one epitope of one antigen. Made in lab or in mice cell cultures.
50
Q

Cytotoxic T-cells (CD8)

A

Directly bind target antgens that are presented by any cell with MHC I.
Releases chemicals that cause cell destruction.

51
Q

Perforins

A

Chemicals secreted by cytotoxic T cells that punch holes in target cell membrane to allow granzymes to center.

52
Q

Granzymes

A

Chemical that induces apoptosis in the target cell.

53
Q

Helper T-cells (CD4)

A

“Alarm” of the immune system. Constantly circulate in the body receive MHC signals and bind to B cells. Secretes cytokines.

54
Q

APCs

A

Dendritic cells, macrophages, Helper T-cells.

55
Q

Cytokine examples

A

(Protein chemical alarm bell)
1. B-Cell growth factor
2. Interleukin 2
3. Chemotaxins
4. Macrophage-migration inhibition factor

56
Q

Suppressor T-Cells

A

Shuts off the immune response when the threat has passed.

57
Q

Receptor editing

A

B cell with receptor for our own bodies antigen can change receptor to a non-self version to prevent attack if encountered.

If a foreign antigen looks like a self antigen our immune system may not attack it, which can lead to more infection.

58
Q

MHC molecule makeup

A
  1. The major histocompatibility complex (MHC) is a set of cell surface molecules encoded by a large gene family which controls a major part of the immune system in all vertebrates.
  2. The major function of major histocompatability complexes is to bind to peptide fragments derived from pathogens and display them on the cell surface for recognition by the appropriate T-cells.
  3. Produced by MHC genes. Self antigens that are plasma membrane glycoproteins.
59
Q

T-Cell activation

A
  1. Requires a foreign antigen and MHC I foreign peptide combination.
  2. Normal body cells are protected via this mechanism.
60
Q

Immune surveillance ingredients

A

Interplay of cytotoxic T cells, NK cells, macrophages and interferon.

61
Q

How the immune system responds to cancer.

A
  1. T-cell system recognizes and destroys newly sprung potentially cancerous tumor cells.
  2. NK cells are the first line of defense.
  3. Cytotoxic T cells defend against virus-induced cancers.

** some cancer cells have blocking antibodies that interfere with T cell function.

62
Q

Immune system regulation

A

Regulated by the endocrine and nervous systems via Negative feedback loops.

63
Q

Allergy response

A

acquisition of an inappropriate specific immune reactivity (hypersensitivity) to a normal harmless environmental substance.

64
Q

Hypersensitivity reactions

A
  1. Type I - IgE mediated
  2. Type II - cytotoxic reaction -mediated by IgG or IgM
  3. Type III - Mediated by immune complexes
  4. Type IV - Delayed - mediated by cellular response.
65
Q

Chemical allergen mediators

A
  1. Histamine
  2. Slow reactive substance of anaphylaxis (SRS-A)
  3. Leukotriene similar to prostoglandins
  4. Eosinophil chemotactic factor
66
Q

Chemical behavior bringing an allergic response

A
  1. IgE anitbody response
  2. Mast cell and basophil reaction
  3. These cells store and release histamine.
67
Q

Leukocytes function and types

A

The effectors of the immune system.

Most leukocytes arise from stem cells in the bone marrow. Lymphocytes arise from lymphocyte colonies in lymphoid tissue.

  1. Neutrophils
  2. Eosinophils
  3. Basofils
  4. Monocytes
  5. Lymphcytes
    a) B Cells
    b) T Cells
68
Q

How lymphatic system responds to a pathogen ?

A

Pathogens in lymph are filtered by lymph nodes.
Lymphocytes serve as macrophages there.

The spleen performs a similar role on the blood.

69
Q

Inflammation’s underlying goal

A

A nonspecific response to tissue injury and its ultimate goal is bring phagocytes & plasma proteins to invaded or injured area.

70
Q

Neutrophil function in inflammatory response stages

A
  1. Neutrophils or monocytes emigrate from the blood into the area.
  2. They adhere to the inside surface of capillaries by margination.

3.They enter the interstitial spaces by diapedesis.

  1. They are guided to the areas where they are needed by chemotaxis.
71
Q

Innate response stages

A
  1. Neutrophil numbers may increase four or five times.
  2. Monocytes increase at a slower rate, forming macrophages.
  3. Bacteria are marked for destruction by opsonins.
  4. This allows phagocytes to distinguish among normal and foreign/abnormal cells.
  5. The opsonins are antibodies and one of the activated proteins of the complement system.
72
Q

Mediation of the inflammatory response by phagocyte-secreted chemicals

A
  1. nitric oxide (fron macrophages)
  2. lactoferrin (from neutrophils)
  3. histamine (increasing capillary permeability)
  4. kinins (formed from kininogens)
  5. endogenous pyrogen (induces fever development)
  6. leukocyte endogenous mediator (decreases plasma iron)
  7. acute-phase proteins from the liver
73
Q

What suppresses inflammatory responses?

A
  1. Salicylates and glucocorticoid drugs
  2. Nonsteroidal anti-inflammatory drugs (NSAIDs)
  3. Cycloxygenase inhibitors:
  4. Aspirin (Also work by inhibiting histamine release)
  5. Ibuprofen
  6. Glucocorticoids - Suppress almost all aspects of inflammatory. Reduce body’s ability to resist infection
  7. Infliximab (Remicade) or similar, Ab to TNF-α, used against autoimmune diseases, Humira is similar.
  8. Chemotherapy drugs: methotrexate, azathioprine, 6-mercaptopurine.
74
Q

B-lymphocytes

A
  1. Each lymphocyte has surface receptors for binding with one particular type of possible antigens
  2. Antigens stimulate B cells to convert into plasma cells that produce antibodies
  3. Most B cells differentiate into active plasma cells. Other B cells become dormant (memory cells)
75
Q

Cell surface proteins to intiate immune response

A
  1. All cells, bacteria, viruses, fungi, yeast, etc. have proteins on their surface.
  2. These proteins may help with facilitated diffusion, active transport, cell-to-cell communication, etc.
    But some of these proteins are used for cell-to-cell recognition.
  3. Foreign proteins that initiate the immune response are called ANTIGENS
  4. These antigens are found on viruses, bacteria, parasitic worms, pollen, fungi, protozoa, etc.
76
Q

Self vs. non-self

A
  1. When lymphocytes mature, they will bear receptors that are specific to different MHC molecules.
  2. All lymphocytes that bear receptors specific for MHC molecules already present in the body undergo apoptosis (programmed cell death or suicide), so that your body is safe from its own defense system
  3. A failure to destroy lymphocytes with “self” receptors, will cause auto-immune diseases like lupus, MS, etc.
77
Q

Polyclonal Antibodies

A

A mixed group of antibodies – each one binds to a separate epitope of an antigen. Antibodies made in our bodies are usually polyclonal.

78
Q

Lymphocyte antigen presentation process

A
  1. Macrophages can be an antigen-presenting cells. They cluster around an appropriate B-cell clone, making the introduction.
  2. Phagocytosis occurs, processing the raw antigen intracellularly and presenting the processed antigen, exposing it to the outer surface of the macrophage’s plasma membrane.
  3. As a macrophage engulfs and ingests a microbe, it ingests it into antigenic peptides.

Each binds to an MHC molecule

  1. The MHC transports the bound antigen to the cell surface, presenting it to passing lymphocytes
  2. Antigen-presenting macrophages secrete interleukin.

This chemical mediator enhances the differentiation and proliferation of the now-activated B cell clone.

79
Q

T-Lymphocyte functions

A

1.Carry out cell-mediated immunity

  1. Do not secrete Abs, directly bind to targets
  2. Killer T cells release chemicals that destroy targeted cells
  3. Clonal & antigen specific. They acquire receptors in the thymus.
  4. T cells are activated for foreign attack only when on the surface of a cell that carries foreign & self antigens. They learn to recognize foreign antigens only in combination with a person’s own tissue antigens.

A few days are required before T cells are activated to launch a cell-mediated attack.

80
Q

T Cell types

A
  1. Cytotoxic
  2. Helper T cells
81
Q

CD8 Cell attributes

A
  1. Cytotoxic T cells secrete chemicals that destroy target cells. Most frequently they destroy cells infected with viruses.
  2. There is a clone of these cells specific for a particular virus. These T cells bind to the viral antigens and self-antigens on the surfaces of the viral- infected cells.
  3. These cells destroy host cells harboring anything foreign.
  4. The cytotoxic T cells release chemicals that destroy the attacked cell before the virus can enter the nucleus and start to replicate.
  5. Cytotoxic T cells also destroy targeted cells by releasing perforins.

**The exception to this is nerve cells.

82
Q

CD4 Cell attributes

A

1.Helper T cells secrete chemicals that amplify the activity of other immune cells. (Cytokines)

  1. Cytokines spur other immune cells to help ward off the invader and modulate the activity of other immune cells.

Cytokine ex.

a) B-cell growth factor
b) Interleukin 2 (grows immune cells)
c) chemotaxins
d) macrophage-migration inhibition factor

83
Q

Suppressor T Cell

A

Turns off the whole immune response when the threat has passed – conserve energy.

84
Q

Immune tolerance

A
  1. Refers to preventing the immune system from attacking the person’s own tissues.
85
Q

Tolerance Mechanisms

A
  1. Clonal Deletion (Major Mechanism)
    Self Ags seen early in development
    Triggering of the Apoptosis of immature cells. These cells would react with the body’s own proteins.
  2. Clonal Anergy
    lymphocyte must receive two specific signals at the same time for activation.

A single signal from a self-antigen turns off a compatible T cell rendering the cell unresponsive to further exposure to the antigen.

  1. Receptor Editing
    B cell with a receptor for one of the body’s own antigens changes its receptor to a non-self version if it encounters a self antigen.
  2. B Ag Sequestering
    Self molecules are hidden from the immune system. Seen with the eyes and testes

`

86
Q

Autoimmune cause progression

A

Autoimmune diseases arise from a loss of tolerance of self-antigens.

  1. The exposure of normally inaccessible antigens induces an immune attack against them.
    Normal self-antigens can be modified.
  2. There is an exposure of the immune system to a foreign antigen almost structurally identical to a self-antigen.

Some could be related to pregnancy, arising from lingering fetal cells in the mother’s body after the pregnancy.

87
Q

Tolerance with MHC

A

MHC molecules on cells block T cell binding.

  1. Cytotoxic T cells do not bind to MHC self-antigens in the absence of a foreign antigen. Therefore, normal body cells are protected from lethal immune attack.
  2. T cells become active only when they match a given MHC-foreign peptide combination.
  3. Cytotoxic T cells can respond to foreign antigens only in association with class 1 MHC glycoproteins.
  4. Class II MHC glycoproteins, recognized by helper T cells, are confined to the surface of a few special types of immune cells.
88
Q

Immune Surviellence

A

The T cell system recognizes and destroys newly arisen, potentially cancerous tumor cells.

  1. Immune surveillance depends on the interplay of cytotoxic T cells, NK cells, and macrophages plus interferon. They attack and destroy cancer cells.
89
Q

Cancer surviellence

A
  1. NK cells are the first line of defense against cancer.
  2. Cytotoxic T cells probably defend against virus-induced cancers.
  3. Macrophages clear away the remains of dead cells and engulf and destroy cancer cells intracellularly.
  4. Some cancer cells have counter-productive blocking antibodies that interfere with T cell function.
90
Q

Immune system regulation mechanisms

A
  1. The immune system is regulated by the endocrine and nervous systems by negative feedback loops.

For example, cortisol mobilizes the body’s store of metabolic fuel.

  1. Lymphocytes and macrophages are responsive to blood-borne signals.
91
Q

Immune deficiencies

A

Results insufficient immune responses.

  1. The immune system does not respond adequately to foreign invasion.
  2. In severe combined immunodeficiency both B and T cells are lacking.

ex. In HIV a virus invades and incapacitates helper T cells.

92
Q

Inappropriate adaptive immune responses

A
  1. They include autoimmune responses, in which the immune system turns against the body.
  2. Another example is immune complex diseases, which damage tissues by violent reactions.
93
Q

Allergy

A
  1. The acquisition of an inappropriate specific immune reactivity (hypersensitivity) to a normally harmless environmental substance.
  2. Hypersensitivity can be immediate (within about 20 minutes after exposure to an allergen) or delayed, occurring a day or so after exposure. Antibody Mediated

The difference is due to different mediators involved.

94
Q

Chemical Mediators of Allergies

A
  1. Histamine
  2. Slow-reactive substance of anaphylaxis (SRS-A), a leukotriene similar to prostaglandins
  3. Eosinophil chemotactic factor
  4. Allergens bind to and elicit the synthesis of IgE antibodies.
  5. Their tail portions are attached to mast cells and basophils.
  6. These cells produce and store inflammatory chemicals such as histamine.

Pathophysiology (11 decks)

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