Chapter 22 - Immunity

Question 1

What are the 5 major categories of pathogens (infectious agents that cause harm to host)?

Answer 1

1.) Bacteria
2.) Virus
3.) Fungi
4.) Protozoans
5.) Multicellular parasites

Question 2

Bacteria

Answer 2

• Prokaryotic and unicellular
• Sticky polysaccharide capsule
• Hairlike pili
• Lack a nuclear envelope but cytoplasm and DNA is enclosed by a plasma membrane and cell wall
• Capsule increases virulence (ability to cause serious illness)
• Some produce enzymes and/or toxins
• Ex diseases: Streptococcal infections, staphylococcal infections, tuberculosis, syphilis, lyme disease, salmonella, anthrax

Question 3

Viruses

Answer 3

• Not a cell and are smaller –> DNA or RNA in capsid protein (may also be within membrane)
• Must enter cell to replicate (obligate intracellular parasites)
• Ex diseases: Cold, influenza, COVID, polio, mumps, measles, hepatitis, rubella, chicken pox, herpes

Question 4

Fungi

Answer 4

• Eukaryotic with cell wall
• Unicellular or multicellular organisms
• Produce spores
• Release proteolytic enzymes (protein-digesting enzymes that induces inflammation, leading to redness and swelling of infected area)
• Fungal diseases (mycoses) in healthy people are usually limited to superficial infections
• Ex diseases: Ringworm, diper rash, athlete’s foot, histoplasmosis

Question 5

Protozoans

Answer 5

• Eukaryotic and lack a cell wall
• Unicellular parasites that interfere with normal cellular functions
• Ex diseases: Malaria, toxoplasmosis, aboebiasis

Question 6

Multicellular Parasites

Answer 6

• Eukaryotic
• Multicellular organisms that live within a host
• Nonmicroscopic
• Ex diseases: Parasitic infections from tape worms, lung flukes, hookworms

Question 7

Prions

Answer 7

• Small fragments of infectious protiens that cause disease in nervous tissue
• Ex: mad cow disease
• Neither cells nor viruses

Question 8

Name the 2 intrinsic systems of immunity

Answer 8

1.) Innate (nonspecific) defense system: present at birth
2.) Adaptive (specific) defense system: Acquired/specific immunity

Question 9

Innate immunity (nonspecific)

Answer 9

Innate immunity: provided by multiple components that protect against a wide variety of substances
- Born with the defenses –> don’t require previous exposure to a foreign substance
- Respond immediately to any potentially harmful agent
- Have specific pathways for certain substances
- Release proteins that alert cells of adaptive system to foreign molecules
First line of defense: Skin and mucosal membranes (prevent entry)
Second line of defense: Most immune cells (macrophages, NK cells, phagocytes, etc., except T/B-lymphocytes), chemicals (interferon, complement, antimicrobial proteins), physiologic responses (ex: inflammation, fever)
- Inflammation is most important

Question 10

Adaptive (specific) immunity

Answer 10

Adaptive immunity: Provided by lymphocytes that are activated to replicate and respond when stimulated by a specific antigen
- Acquired immunity –> process begins immediately but development of adaptive immunity against substance takes several days to be effective (longer than innate)
Components include…
1.) T-lymphocytes –> cell-mediated immunity
2.) B-lymphocytes –> antibody-mediated immunity
- Plasma cells (from B-cells) –> synthesize and release antibodies

Question 11

Commensial microbiota (normal microflora)

Answer 11

• Microorganisms that reside on the body surfaces
• Non-pathogenic microorganisms interfere with the attachment and growth of other, potentially more virulent types

Question 12

Adaptive defense system

Answer 12

• Third line of defense attacks particular foreign substances
• Takes longer to react than innate
• More specific to specific pathogens
  1.) Humoral (antibody) immunity –> B cells
  2.) Cellular (cell mediated) immunity –> T cells
• T-Helper cells (Th)
• Cytotoxic T Cells (Tc)

Question 13

Innate defenses - Surface barriers ward off invading pathogens

Answer 13

1.) Skin, nucous membranes, and secretions
- Physical barrier
- Keratin –> Resistant to weak acids and bases, bacterial enzymes, and toxins
- Mucosae provide similar mechanical barriers
2.) Protective chemicals inhibit or destroy microorganisms
- Acidity of skins and secretitions inhibit growth
- Enzymes (lysozyme of saliva, respiratory mucus, and lacrimal fluid) kill many microorganisms
- Defensins (antimicrobial peptides) inhibit growth
- Other chemicals (lipids in debum, dermicidin in sweat) toxic
3.) Respiratory system modifications
- Mucus-coated hairs in nose
- Cillia of upper respiratory tract sweep dust and mucus with bacteria towards mouth

Question 14

Describe the process of making a MCH

Answer 14

• A cell encounters bacteria and engulfs it –> phagosome: Part with engulfed substance
• There is a vesicle with powerful enzymes (lysosome)
• Phagosome and vessicle fuse –> enzymes from lysosome will break apart bacteria
• A protein on cell surface will present bacteria piece –> Major histocompatibility complex (MHC)
  Antigen presenting cell (APC): The name of the overall final cell

Question 15

What are the phagocytic cells?

Answer 15

• Neutrophils (- Phagocytize bacteria, usually arrive first to a scene when there is a breach in defense)
• Macrophages (- Phagocytic cell, Serves as APC for T-lymphocytes, develop from monocytes, chief phagocytic cells, can wander in tissue or live in organs)
• dendritic cells (- Phagocytic cells of skin and mucous membranes)

Question 16

What are the proinflammatory chemical-secreting cells?

Answer 16

• Basophil (- Circulate blood)
• Mast cell (- Reside in connective tissue of the skin, mucosal linings, and internal organs)
• Both enhance inflammation
• Release granules during inflammatory response
  1.) Histamine –> increases vasodilation and capillary permeability
  2.) Heparin –> Anticoagulant
  3.) Eicosanoids –> released from plasma membrane

Question 17

What is the aptosis-initiating cell?

Answer 17

• NK cell
• Located within secondary lymphoid structures
  Immune surveillance: Process of patroling body to detect unhealthy cells
• Cytotoxic chemicals are released –> Perforin (forms pores in plasma membrane) and granzymes (enter cell through transmembrane pore to initiate apoptosis)
  Apoptosis: Cellular death where cell shrinks

Question 18

Parasite-destroying cell

Answer 18

-Eosinophils
- Target cellular parasites and attack organisms surfaces
- Include degranulation and release of enzymes
- Can release proteins that form pores to destroy cells
- Participates in immune responses associated with allergy and asthma

Question 19

How innate immune cells identify micromes (Motifs and TLRs)

Answer 19

• Microbes have a patterned molecular structure (motifs) that they have in common
• Innate immune cells have pattern recognition receptors (Toll-like receptors –> TLRs) on cell surfaces –> will make physical contact with molecular motifs

Question 20

Mechanism of phagocytosis

Answer 20

Is fatal to neutrophils, but macrophages and dendritic cells continue to function after and present fragments on cell surface
1.) Phagocyte adheres to particle
2.) Opsonization marks pathogens (coating by complement protiens or antibodies, making it more attractive for phagocytosis)
3.) Cytoplasmic extensions bind to and engulf particle in vesicle called phagosome
4.) Phagosome fuses with lysosome –> phagolysosome
5.) Pathogens killed by acidifying and digesting with lysosomal enzymes
6.) Indigestible and residual material is removed via exocytosis
Other information:
- Helper T cells cause release of enzymes of a respiratory burst –> kills pathogens resistant to lysosomal enzymes by releasing cell-killing free radicals, producing oxidizing chemicals (ex: H2O2), and increasing pH and osmolarity of phagolysosome
- Defensins (in neutrophils) pierse membrane

Question 21

Natural killer (NK) cells

Answer 21

• Nonphagocytic large granular lymphocytes
• Attack cells that lack “self” cell-surface receptors –> induce apoptosis in cancer and virus-infected cells
• Secrete potent chemicals that enhance inflammatory response

Question 22

Information about inflammation and inflammatory response

Answer 22

Inflammation: An immediate, local, nonspecific event that occurs in vascularized tissue against a variety of injury-causing stimuli
- Triggered whenever body tissues injured
- Prevents spread of damaging agents
- Disposes of cell debris and pathogens
- Alerts adaptive immune system
- 4 cardinal signs of acute inflammation
1.) Redness from increased blood flow
2). Heat from increased blood flow and metabolic activity in area
3.) Swelling from increase in fluid loss from capillaries
4.) Pain from stimulation of pain receptors
Sometimes 5–> impairment of function if movement is hampered from pain and swelling

Question 23

Steps of inflammation

Answer 23

1.) Release of inflammatory and chemotactic factors
- Damaged cells release chemicals that promote inflammation (ex: histamine, leukotrienes, prostaflandins, interleukins, TNFs, chemotactic factors)
2.) Vascular changes
- Vasodilation of arterioles
- In crease in capillary permeability
- Displayh of CAMS (cell-adhesion molecules)
3.) Recruitment of leukocytes
- Margination –> CAMS on leukocytes adhere to CSMS on endothelial cells of capillaries within injured tissue
- Diapedesis –> Leukocutes exit the blood between endothelial cells and micrate to infection site
- chemotaxis –> Migration of leukocytes along a chemical gradient (leukocytes may release cytokines)
4.) Delivery of plasma proteins
- Selective plasma proteins are brought into site
Kinins: produced from kininogen –> inactive plasma protiens produced by liver –> have smiliar effects to histamine –> promote production of CAMS by the capillary endothelium –> most significant stimulus for causing the pain associated with inflammation

Question 24

Antimicrobial proteins

Answer 24

• include interferons (IFNs) and complement proteins
• Attack microorganisms directly
• Hinder microorganisms ability to reproduce

Question 25

Interferons

Answer 25

- Family of immune modulating proteins - VIral-infected cells secrete IFNs to warn neighboring cells - IFNs enter neighboring cells and produce protens that block viral reproduction and degrade viral RNA - IFN ⍺ and β can activate NK cells - IFN gamma (immune interferon) --> secreted by lymphocytes, widespread immune mobilizing affects, activates macrophages

Question 26

Complement system

Answer 26

- ~20 blood proteins that circulate in inactive form and produced by liver - Work along w/ "complement" antibodies - Unleashes inflammatory chemicals that amplify all aspects of inflammatory response - Kills bacteria and cells by cell lysis - Enhances innate and adaptive defenses Classical pathway/complement fixation: Antibodies bind to invading organisms and to complement components, first step in activation --> Complement protein binds to an antibody Alternative pathway: Triggered when activated C3, B, D, and P interact on surface of microorganisms --> Surface polysaccharides of certain bacterial and fungal cell walls bind directly with a complement protein Lectin pathway: Lectins produced by innate system to recognize foreign invaders --> when bound by foreign invaders, can also bind and activate complement (Mannan-binding lecting produced by the liver binds to specific carbohydrates on certain microorganisms)

Question 27

Opsonization

Answer 27

The binding of a protein (ex: complement) to a portion of bacteria/other cell type to enhance phagocytosis - Opsonin: The binding protein --> functions as a red flag

Question 28

Membrane attach complex (MAC)

Answer 28

A protein channel formed in the plasma membrane of a target cell - Part of direct killing triggered by complement components like C5-9 - Compromises cell's integrity

Question 29

Fever (Pyrexia)

Answer 29

- Results from pyrogens (fever-inducing molecules that are released from either infectious agents or immune cells in response to infection, trauma, etc) - ABnormally high body temp, 1C or more from normal (37C/98.6F) - Leukocytes and macrophages exposed to foreign substances secrete pyrogens (ex: IL-1) from immune cells or infectious agents - Pyrogens act on body's thermostat in hypothalamus, raising the body temperature as microorganisms may have better replication rate at higher temp

Question 30

Benefits of moderate fever

Answer 30

- Causes liver and spleen to hold onto iron and zinc (needed by microorganisms) - Increases metabolic rate --> faster repair

Question 31

Abnormally high body temp vs moderate fever

Answer 31

High body temp --> May be because of molecules released from microorganisms Moderate fever --> May be because of molecules released by our WBC and can slow down replication of invaders

Question 32

Events of a fever

Answer 32

1.) Onset: Pyrogens are released from various types of cells and circulate the blood - Target hypothalamus and cause release of prostaglandin E2 (PGE2) - a local hormone - Raises temperature set point of the hypothalamus from normal - Hypothalamus stimulates blood vessels in dermis of skin to vasoconstrict --> increasing body temperature and can lead to chills 2.) Stadium - The period of time when the elevated temperature is maintained - Metabolic rate increases to promote process of innate and adaptive immunity 3.) Defervescence: Occurs as the temperature returns to its normal set point - Fever breaking - Hypothalamus is no longer stimulated by pyrogens - Postaglandin release decreases - Hypothalamus stimulates the mechanisms to release heat from body

Question 33

Risks of different fever levels

Answer 33

Low-grade fever: ~100 - 1001 F Intermediate grade fever: ~ 102F - Seizures may occur if sustained >102 High-grade fever: ~ 103 - 104F - Can be dangerous because of protein denaturation Dangerous high-grade fevers: ~>104F - Irreversable brain damage at sustained >106F - Convulsions and death at 108F

Question 34

The branches of adaptive immunity

Answer 34

1.) Humoral immunity - T-lymphocytes --> effective against antigen within cells and requires antigen presenting cell - Cytotoxic T-Lymphocyte (destroys cells through apoptosis) - Helper T-Lymphocyte (releases molecules like interleukins that regulate immune system) 2.) Antibody mediated immunity - B-lymphocytes --> effective against antigen outside cells, doesn't require antigen-presenting cell - Plasma cells (produce antibodies)

Question 35

Antigens

Answer 35

- Can provike an immune resposne and most are large, complex molecules not normally found in body - Include tumor antigens, foreign antigens, and self-antigens

Question 36

Hepatins

Answer 36

- Incomplete antigens - Small molecules not immunogenic by themselves and too small to function an antigen alone - Become immunogenic when attached to carrier molecule Causes immune system to mount harmful attack - Ex: poison ivy, detergents, cosmetics

Question 37

Antigenic determinants

Answer 37

- Also called epitope - Each has different shape - Only certain parts of entire antigen are immunogenic (antigenic determinants) - Antibodies and lymphocyte receptors bind to them as enzyme binds substrate

Question 38

Major histocompatibility complex (MHC)

Answer 38

- Self-antigens on surface of cells not antigenic to self but antigenic to others in transfusions or grafts - Ex: MHC glycoproteins--> coded by genes of MHC and unique to individual, have grove holding self-/foreign- antigen, lymphocytes only bind anitgens on MHC proteins

Question 39

Cells of adaptive immune system

Answer 39

1.) Lymphocytes - B lymphocytes --> Humoral immunity - T lymphocytes --> cell-mediated immunity 2.) Antigen-presenting cells (APCs) - Don't respond to specific antigens

Question 40

General Lymphocyte development

Answer 40

1.) Origin at red bone marrow 2.) Maturation 3.) Seeding secondary lymphoid organs and circulation 4.) Antigen encounter and activation 5.) Proliferation and differentiation

Question 41

Thymix selection process

Answer 41

- Process thymocytes (pre T-lymphocytes) go through in thymus to mature 1.) Positive selection: Survival dependent on ability to bind to MHC molecule - Occurs in outer thymus cortex - Receptor complex on membrane (CD4 and CD8) must bind to an MHC molecule - If they pass, they go into the medulla of thymus 2.) Negative selection: Survival dependent upon not recognizing self-antigen -Must not bind to self antigens - Tested by thymic dendritic cells presenting self-antigens with MHC class 1 and 2 molecules - Self-tolerance: State of ignoring self-antigens --> primarily occurs at primary lymphoid structures 3.) Selective loss of either CD4 or CD8 proteins - By this point, 2% of cells survive selection process - Determined by how tightly CD4 receptors are able to bind the MHC class 2 molecules - Bind tightly = become CD4 cells - Not tight = Become CD8 cells 4.) Immunocompetent B and T cells not yet exposed to antigen --> Naive -- > exported from primary lymphoid organs (bone marrow and thymus) to "seed" secondary lymphoid organs --> increases chances of encounter with antigen

Question 42

Clonial selection

Answer 42

- Process of forming a clone in response to a specific antigen Antigen challenge: The first encounter between an antigen and lymphocyte --> Occurs in secondary lymphoid structure - Naive lymphocytes first encounter with antigen --> selected for further development - If correct signals present, lymphocyte will complete its differentiation

Question 43

Lymphocyte recirculation

Answer 43

- Lymphocytes reside only temporarily in any given secondary lymphoid structure and then circulate through blood/lymph every several days - Makes it likely to encounter its antigen

Question 44

TCR/BCR

Answer 44

- T-cell receptor --> The antigen receptor of a T-lymphocyte - B-cell receptor --> The antigen receptor of a B lymphocyte

Question 45

Double positive and double negative thymocytes

Answer 45

Double negative: Possess a unique TCR and initially have neither CD4/CD8 Double positive: In thyms, produce both CD4/CD8

Question 46

Immunocopetence

Answer 46

Lymphocyte can recognize one specific antigen by binding to it - B/T cells display unique receptor on surface when achieve maturity --> binds only one antigen

Question 47

Self tolerance

Answer 47

Lymphocytes unresponsive to own antigens

Question 48

Effector response

Answer 48

- The mechanisms that activated lymphocytes use to help eliminate the agent

Question 49

Effector response of helper T-lymphocytes

Answer 49

- Activated and memory leave secondary lymphoid structure after days exposed to antigen - Migrate to infection site and release cytokines to regulate other immune cells - Enhance activation of cytotoxic T-lymph through release of cytokines (ex: IL-2) - Enhance formation of activity of cells providing innate immunity (ex: macrophages, NK cells)

Question 50

Effector repsonse of cytotoxic T-cells

Answer 50

- Activated and memory leave secondary lymphoid structure after days of antigen exposure - Destroy unhealthy cells that display an antigen - Effector repsonse is initiated when physical contact is made between a cytotoxic T-lymphocyte and the specific foreign antigen displayed with MHC class 1 molecules of an anhealthy or foreign cell - Destroys via apoptosis ---> release granules with perforin and granzymes (enters cell through perforin channels and induce apoptosis)

Question 51

Effector response of B-lymphocytes

Answer 51

- Following maturation into plasma cells - Form antibodies and provide antibody mediated immunity --> come into contact with antigen at infection site - Antibodies are formed primarily by plasma cells, limited made by B-lymphocytes - Plasma cells remain in lymph nodes Antibody titer: The circulating blood concentration of antibody specific antigen --> a measure of immune response