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Anatomy and Physiology > immune iii > Flashcards

immune iii Flashcards

1
Q

Antibodies

A
  • immunoglobulins = gamma globulin portion of blood
  • proteins secreted by plasma cells
  • capable of binding specifically with antigen detected by B cells
  • grouped into 5 Ig classes
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2
Q

Antibody structure

A
  • T or Y shaped antibody monomer of 4 looping polypeptide chains linked by disulfide bonds
  • 2 heavy chains with hinge region at “middles”
  • two identical light chains
  • variable regions at one end of each arm combine to form two identical antigen-binding sites
  • Constant regions of stem determine antibody class and serve common funcs in all antibodies
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3
Q

IgM

A
  • Pentamer (biggest)
  • 1st antibody released
  • potent agglutinating agent
  • readily fixes and acticates complement
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4
Q

IgA

A
  • secratory IgA
  • monomer or dimer
  • in mucus, breast milk, and other secretions
  • helps prevent entry of pathogens
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5
Q

IgD

A
  • Monomer attached to surface of B cells

- Functions as B cell receptor

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6
Q

IgG

A
  • monomer
  • 75-85% of antibodies in plasma
  • from secondary and late primary responses
  • crosses placental barrier
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7
Q

IgE

A
  • monomer active in some allergies and parasitic infections

- causes mast cells and basophils to release histamine

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8
Q

B cell specieal antibody skill

A
  • B cells can switch antibody classes, but retain antigen specificity
  • IgM at first, then IgG
  • almost all secondary responses are IgG
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9
Q

Antibody targets and functions

A
  • antibodies inactivate and tag antigens; do not destroy them –> form antigen-antibody complexes
  • defensive mechanisms used by antibodies: neutralization, agglutination, precipitation, and complement fixation
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10
Q

Neutralization

A
  • simplest defensive mechanism
  • antibodies block specific sites on viruses or bacterial exotoxins
  • prevent these antigens from binding to receptors on tissue cells
  • antigen-antibody comlexes undergo phagocytosis
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11
Q

agglutination

A
  • antibodies bind same determinant on more than one cell-bound antigen
  • cross-linked antigen-antibody complexes agglutinate (e.g. clumping of mismatched blood cells)
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12
Q

Precipitation

A
  • soluble molecules are cross-linked

- complexes precipitate and are subject to phagocytosis

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13
Q

Complement fixation and activation

A
  • main antibody defense against cellular antigens (bacteria or mismatched RBCs)
  • several antibodies bind close together on a cellular antigen –> complement-binding sites on stem regions of antibodies align –> triggers complement fixation to cells surface –> cell lysis
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14
Q

activated complement functions

A
  • amplifies inflammatory response
  • promotes phagocytosis via opsonization –>positive feedback cycle that enlists more and more defensive elements
  • activated complement forma MAC

Example of adaptive immune response enhancing innate response

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15
Q

Cell mediated immunity: activation of T cells

A

first signal in activation:

  • T cell receptors recognize and bind to a specific foreign antigen fragment that’s presented in antigen-MHC complexes
  • CD4 and CD8 proteins are coreceptors

second signal required for activation

  • costiulation: 20 known substances (cytokines, plasma membrane molecules)
  • may prevent immune response from occuring accidentally
  • anergy = recognition without costimulation (in both B and T cells) –> leads to prolonged state of inactivity
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16
Q

Activation and clonal selection of helper T cells

A
  • most that display CD4 develop into helper T cells –> some become regulatory T cells which moderate immunne response
  • recognize exogenous antigen fragments associated with MHC-II molecules on the surface of an APC
  • after activation, undergoes clonal selection
  • Makes active helper T cells and memory helper T cells
  • Active hleper T cells secrete cytokines (interleukin 2 needed for all immue resposes)
  • Memory helper t cells aren’t active –> can quickly proliferate and differentiate if the antigen appears again
17
Q

Activation and clonal selection of cytotoxic t cells

A
  • most taht display CD8 develop into cytotoxic T cells (CD8 T cells)
  • recognize antigens combined with MHC-I
  • Maximal activation also requires presentation of antigen with MHC-II to cause helper T cells to make IL-2
  • Undergoes clonal selection
  • Active cytotoxic T cells attack body cells
  • Memory cytotoxic T cells don’t attack, but wait for an antigen to appear again
18
Q

Elimination of invaders

A
  • cytotoxic T cells migrate to seek out and destroy infected target cells
  • kill like NK cells
  • major difference is T cells have specific receptor for particular microbe, but NK cells eat a ton of stuff

2 ways to kill: granzyes cause apoptosis; perforin and/or granulysin causes cytolysis

19
Q

immunological surveillance

A

tumor antigens displayed on cancerous cells targeted by cytotoxic T cells, macrophages, and NK cells

20
Q

Roles of helper T cells

A
  • central role in adaptive immunne response
  • activate both humoral and cellular arms
  • once primed by APC presentation of antigen they help activate T and B cells, induce T and B cell proliferation, and their cytokines recruit other immune cells

Without helper T cells, there’s no immune response

21
Q

Helper T cells’ activation of B cells

A
  • interact directly with B cells displaying antigen fragments bound to MHC II receptors
  • release cytokines to stimulate B cells to divide more rapidly and begin atibody formation
  • B cells may be activated without helper t cells by binding to T cell-independent intigens (response is weak and short, though)
  • Most antigens require helper T cell co-stimulation to activate B cells: T cell-dependent antigens
22
Q

Helper T cell activation of CD8 cells

A
  • CD8 cells require hleper T cell activation into destructive cytotoxic T cells
  • cause dendritic cells to express co-stimulatory molecules required for CD8 cell activation
23
Q

Helper T cells amplification of innate defenses

A
  • amplify responses of innate immune system
  • activate macrophages –> more potent killers
  • mobilize lymphocytes and macrophages and attract other types of WBCs
24
Q

Hypersensitivities

A
  • immune responses to perceived threat cause tissue damage
  • different types distinguished by their time course and whether antibodies or T cells involved
  • Antibodies cause immediate and subacute hypersensitivities
  • T cells cause delayed hypersensitivity
25
Q

Subacute Hypersensitivities

A
  • caused by IgM and IgG transferred via blood plasma or serum
  • slow onset (1-3 hours) and long duration (10-15 hours)

Cytotoxic (type II) reactions

  • antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement-mediated lysis of cellular antigens
  • example: mismatched blood transfusion
26
Q

Delayed hypersensitivities (type IV)

A
  • slow onset (1-3 days)
  • mechanism depends on helper T cells
  • cytokine-activated macrophages and cytotoxic T cells cause damage
  • example: allergic contact dermatitis (e.g. poison ivy)
  • agents act as haptens
  • TB skin test depends on this reaction
27
Q

Acquired immue deficiency syndrome (AIDs)

A
  • Cripples immune system by interfering with activity of helper T cells
  • characterized by severe weight loss, night sweats, and swollen lymph nodes
  • opportunistic infections occur, including pneumocystis pneumonia and Kaposi’s sarcoma
28
Q

AIDs and HIV

A
  • caused by human immunodeficiency virus (HIV) transmitted via body fluids (blood, semen, and vaginal secretions)
  • HIV enters blood via blood transfusions, blood contaminated needles, sexual intercourse and oral sex, mother to fetus
  • HIV destroys hleper T cells and depresses cellular immunity
29
Q

autoimmune diseases

A
  • immune system loses ability to distinguish self from foreign
  • production of autoantibodies and sensitized Tc cells taht destroy body tissues

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