Adaptive Defenses Study Guide Flashcards

1
Q

two arms of adaptive immunity + what lymphocytes play a role in each

A
  • humoral/antibody mediated immunity - b cells
  • cellular/cell-mediated immunity - t cells
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2
Q

humoral/antibody mediated immunity

A
  • “Antibody Mediated”
  • Immunity is provided by antibodies in the body’s fluids - blood and lymph
  • Antibodies are produced by lymphocytes but circulate freely
  • Antibodies bind to extracellular targets and mark them for destruction by phagocytes
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3
Q

cellular/cell-mediated immunity

A
  • Protection provided by lymphocytes
  • The targets are cells infected by pathogens, cancer cells, or cells of foreign grafts
  • Lymphocytes attack directly by killing the infected cells or indirectly by releasing chemicals
  • Chemicals enhance the inflammatory response or activate macrophages
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4
Q

What type of lymphocyte produces antibodies?

A

B lymphocytes of the humoral immunity

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5
Q

How do antibodies fight invasion?

A

Antibodies bind to extracellular targets and mark them for destruction by phagocytes

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6
Q

What kinds of cells are targeted in cell-mediated immunity?

A

Cells infected by pathogens, cancer cells, or cells of foreign grafts

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7
Q

4 characteristics of adaptive immunity

A
  • It involves *lymphocytes: B-Cells and T-Cells
  • It is *specific: recognizes and targets identified pathogens/foreign substances
  • is it *systemic: not restricted to the initial infection site
  • It has *memory: after priming, it can mount stronger attacks
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8
Q

Antigens

A

antibody generating – they are large, unfamiliar, complex molecules that are intruders or non-self. They are substances that can mobilize adaptive defenses. Complete antigens have immunogenicity – the ability to stimulate specific lymphocytes to proliferate, and reactivity – the ability to react with activated lymphocytes.

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9
Q

Haptens

A

trouble some small molecules, incomplete antigens. Ex – chemicals found in poison ivy, animal dander, detergents, cosmetics, household products

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10
Q

Is it possible for antigens to provoke immune responses in more than 1 type of leukocyte? how?

A

Many antigens have a variety of antigenic determinants (the specific parts of the antigen that are immunogenic) on their surface, so they have the ability to mobilize multiple leukocyte populations and produce multiple types of antibodies

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11
Q

role of an APC

A

Antigen presenting cell – play auxiliary roles – they do not directly respond to antigens

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12
Q

type of lymphocyte especially reliant on APCs

A

T cells (lymphocytes) cannot recognize antigens without apcs

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13
Q

5 steps of lymphocyte development

A
  1. Origin: Originate in red bone marrow - from what?
  2. Maturation: Cells are “educated” to develop immunocompetence and self-tolerance
    Immunocompetence: ability recognize one specific antigen - once achieved, a unique antigen receptor is displayed on the lymphocyte’s surface
    Maturation of B-Cells occurs in Bone Marrow
    Maturation of T-Cells occurs in the Thymus
  3. Seeding Secondary Lymphoid Organs: naive but immunocompetent B-Cells and T-Cells migrate to 2ndary lymphoid organs and await encounters with antigen
  4. Antigen Encounter and Activation: antigen binds to the lymphocyte that has its receptor; that lymphocyte is selected for further development - clonal selection
  5. Proliferation and Differentiation: once activated, the lymphocyte rapidly proliferates to form an army of cells (“a clone”) just like itself - with the same antigen specificity
    Most members of the clone become effectors (infection-fighting) cells, but some will become memory cells
    Memory cells will lie in wait for a subsequent encounter with the same antigen
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14
Q

positive selection test in lymphocytes

A

the maturing lymphocyte must be able to recognize the MHC (inability to do this = apoptosis)

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15
Q

negative selection tests for lymphocytes

A

the maturing lymphocyte must not recognize self-antigen (recognizing self antigen = apoptosis)

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16
Q

What determines the diversity of our antigen receptors?

A

Our genes – not the antigens we encounter – determine which specific foreign substances our immune system will be able to recognize and resist; the diversity of receptors on our lymphocytes represents genetically acquired knowledge of the microbes likely to be in our environment

17
Q

The effector B-Cell is called a __________.

A

plasma cell

18
Q

plasma cells

A

They secrete antibodies that circulate in blood or lymph where they bind to free antigen and mark them for destruction

19
Q

What becomes of the non-effector B-Cells?

A

become memory cells – memory cells can mount an almost immediate humoral response when the same antigen is encountered in the future

20
Q

What are the effector T-Cells?

A

Cytotoxic t (tc) cells
Helper t (th) cells
Regulatory t (treg) cells

21
Q

Primary Immune Response

A

occurs on 1st exposure to antigen
- 3-6 day lag time
- B-cells specific to that antigen proliferate, offspring differentiates into antibody-secreting plasma cells
- Plasma antibody levels peak in about 10 days then decline

22
Q

Secondary Immune Response

A

occurs on any subsequent exposure to the same antigen
- Response is faster, more prolonged, and more effective; “priming” has already occurred
- 2-3 day lag time
- Plasma antibody concentrations rise sharply to much higher levels than the primary response
- Plasma antibody concentrations remain high for weeks to months
- Memory cells persist for long periods - can retain capacity to produce powerful humoral responses for life

23
Q

Active Humoral Immunity

A

your B-cells encounter antigens and produce antibodies against them
- can be natural or artificial

24
Q

natural active immunity

A

you contract a bacterial or viral infection, experience symptoms, and develop antibodies

25
Q

artificial active immunity

A

you receive a vaccine to prime your immune system

26
Q

Passive Humoral Immunity

A

ready-made antibodies are introduced - B-cells are not challenged, immunological memory does not occur
- can be natural or artificial

27
Q

Natural Passive Immunity

A

conferred on a fetus or infant when maternal antibodies cross the placenta or are ingested in breast milk

28
Q

Artificial Passive Immunity

A

administration of a donor’s antibodies - can be used to treat Hepatitis A, poisonous snake bites, rabies, and tetanus

29
Q

What type of immunity is garnered through a vaccine?

A

Artificial active immunity

30
Q

What role do booster shots play?

A

intensify the immune response

31
Q

What portion of an antibody is responsible for forming antigen-antibody complexes?

A

Variable regions – antibodies responding to different antigens have different variable regions

32
Q

defense mechanisms of antibodies

A

Neutralization
Agglutination
Precipitation
Complement Activation (Lysis)

33
Q

Neutralization

A

antibodies block specific sites on pathogens to prevent attachment to tissue cells - phagocytes destroy antigen-antibody complexes

34
Q

Agglutination

A

antigen-antibody complexes are cross-linked into large latices

35
Q

Precipitation

A

soluble molecules are cross-linked into large lattices that fall out of solution - once settled, soluble molecules are eaten by phagocytes

36
Q

Complement Activation (Lysis)

A

several antibodies bind close together on a cellular antigen and complement is activated - membrane attack complexes insert into the antigenic cell’s surface and cell lysis occurs

37
Q

Why are MHC proteins important?

A
  • Major histocompatibility complex – proteins that help identify a cell as “self”
  • Contain a self or foreign antigen
  • Only identical twins have the same mhc
  • T cells can only recognize antigens that are presented on mhc proteins
  • Our self antigens are not antigenic to us, but highly antigenic to others
38
Q

difference in CD4 and CD8 cells

A

Cd4 can only bind with mhc II and cd8 can only bind with mhc I