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HSS 3305 > Lecture 7 > Flashcards

Lecture 7 Flashcards

1
Q

What are the 2 branches of adaptive immunity?

A

Humoral (B-cells) and Cell-mediated (T-cells - CD4, CD8)

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2
Q

Humoral immunity

A

Antibody production, Main defence against bacteria and bacterial toxins

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3
Q

Cell-mediated Immunity

A

Formation of a population of lymphocytes that attack and destroy infected cells (CD8), Main defense against viruses, fungi, parasites, cancers, and some bacteria, rejection of transplanted organs,

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4
Q

Chain of events when a foreign antigen enters the body

A
  • Recognition of foreign antigen
  • Proliferation of individual lymphocytes that are programmed to respond to the antigen form a large group (clone) of cells
  • Destruction of pathogen /infected cells by the responding lymphocytes
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5
Q

T lymphocyte Response

A

Unable to respond to a foreign antigen (TCR) until a macrophage or dendritic cell (APC) cell has phagocytosed the antigen, digested it, and displayed on its cell membrane the antigen fragments combined with its own MHC proteins

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6
Q

B Lymphocyte Response to antigen

A
  • Have immunoglobulin molecules (BCR) on their cell membranes that function as antigen receptors, and they can bind entire antigen molecules to their receptors (do not require MHC presentation)
  • Processed into fragments
  • Fragments displayed on the cell’s membrane with MHC class ll proteins for presentation and recognition by CD4 T-cells to enhance antibody production
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7
Q

Antibodies

A

Globulins produced by plasma cells and can only recreate to specific antigen that induce its formation

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8
Q

Antibody function

A
  • Activation of complement
  • Neutralization
  • Agglutination
  • Opsonization
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9
Q

Types of antibodies

A
  • Immunoglobulin G (IgG)
  • Immunoglobulin A (IgA)
  • Immunoglobulin M (IgM)
  • Immunoglobulin E (IgE)
  • Immunoglobulin D (IgD)
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10
Q

IgG

A
  • Smaller antibody
  • Principal antibody molecule in response to majority of infectious agents
  • Monomer shape
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11
Q

IgM

A
  • Large antibody; a macroglobulin – early production before IgG is produced
  • Responsible for immune control in early response
  • Expressed on surface as monomer – secreted form (pentamer)
  • Very efficient combining with fungi
  • Pentamer
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12
Q

IgE

A
  • Found in minute quantities in blood; binds to mast cells, basophils/eosinophils
  • Concentration is increased in allergic individuals
  • Important in controlling parasitic infections
  • Monomer
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13
Q

IgA

A
  • Produced by antibody-forming cells located in the respiratory and gastrointestinal mucosa (GI/respiratory and urogenital tract)
  • Combines with harmful ingested or inhaled antigens, forming antigen–antibody complexes
  • Dimer
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14
Q

IgD

A
  • Found on cell membrane of B lymphocytes (Functions mainly as BCR) - no plasma cell
  • Present in minute quantities in blood
  • Monomer
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15
Q

What type of immunoglobulins are on Naïve B cells on their cell surface

A

IgM and IgD

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16
Q

What do plasma cells do?

A
  • Proliferation/Increased Ab production
  • Class switching – specialized effector functions.
  • Affinity Maturation – competition/ mutation
  • Memory (travel to spleen/BM)
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17
Q

Why do B-cells need T-cells

A

Ab production is weak and short lived with no memory

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18
Q

Methods of adaptive immunity control

A
  • Cytokines (direct/control immune response)
    -Tolerance (central/peripheral)
    -Regulatory cells
    -Activation vs. Anergy/Apoptosis
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19
Q

Loss of control of Adaptive Immunity

A

Hypersensitivity or Autoimmunity

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20
Q

Cytokine for cell-mediated immunity

A

IL-2

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21
Q

Cytokines for Humoral immunity

A

IL-4 and IL-5

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22
Q

IL-2

A

• Interleukin 2 is produced by T cells, It is the major growth factor for T cells. Also promotes the growth of B cells
• IL-2 acts on T cells in paracrine/autocrine fashion.
• Activation of T cells results in expression of IL-2R and the production of IL-2. promotes cell division.

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23
Q

IL-4

A

• Interleukin 4 is produced by macrophages and Th2 cells.
• stimulates the development of Th2 cells from naïve Th cells and it promotes the growth of differentiated Th2 cells resulting in the production of an antibody response.

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24
Q

IL-5

A

Interleukin 5 is produced by Th2 cells and it functions to promote the growth and differentiation of B cells and eosinophils. It also activates mature eosinophils.

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25
Q

TGF-Beta

A

• Transforming growth factor beta is produced by T cells and many other cell types. It is primarily an inhibitory cytokine.
• It inhibits the proliferation of T cells and the activation of macrophages. It also acts on cells to block the effects of pro-inflammatory cytokines.

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26
Q

INF-y

A

• Interferon gamma is an important cytokine produced by primarily by Th1 cells, although it can also be produced by Tc and NK cells to a lesser extent.
• It has numerous functions in both the innate and adaptive immune systems.

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27
Q

Th1 pathogens

A

-(cell based) geared towards viral/ bacterial attacks in blood/ tissues
-Polarize cells of adaptive and innate immunity to promote cellular immunity most effective against these invaders –PROINFLAMMATORY

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28
Q

Th2 pathogens

A

-(humoral-antibody) geared towards parasitic/mucosal infections.
-ANTIIFLAMMATORY
-Antibody based
-basis of hygiene
-Hypothesis, Allergy IgE

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29
Q

Cytokine Positive feedback

A

Th1/2 cytokines enhance and encourage Th1/2 functions and uncommitted cells (IL-2/IL-4)

30
Q

Cytokine Negative feedback

A

Th1 inhibits Th2 functions and vice versa (IFNgamma/IL-10)

31
Q

Central Tolerance

A

T and B cells must not react to self antigens and be restricted to self MHC molecules

32
Q

Where do Immature T-cells go?

A

They go from bone marrow to the thymus from the blood

33
Q

How to TCRs remain diverse

A

They proliferate and rearrange gene segments

34
Q

Positive selection - MHC

A

Cells that recognize MHC-peptide complexes receive rescue signals that prevent apoptosis

35
Q

Negative Selection - self cells

A

Cells that survive positive selection exit the thymic cortex to the medulla where they are tested for tolerance to self-antigens

36
Q

AIRE(autoimmune regulator) gene

A

Causes transcription of a wide selection of organ-specific genes that create proteins that are usually only expressed in peripheral tissues

37
Q

Fetal development

A

Full complement when born, activity of thymus decreases over time with large drop in thymic function after puberty

38
Q

B-cells central tolerance

A

Decreased stringency of central tolerances mechanism compared to T-cells. B-cells continue to develop throughout life

39
Q

Positive B-cell selection

A

Activate B-cell maturation

40
Q

Negative B-Cell selection

A

Reaction to self

41
Q

Peripheral Tolerance

A

Naïve T-cells stay in circulation, don’t stay in LN, or tissues so they only encounter a portion of the antigens in our body (compartmentalization)

42
Q

Cell Anergy

A

Apoptosis; shut off the immune response (indirectly and directly)

43
Q

Indirect cell anergy

A

Fewer antigens present to stimulate an immune response (DCs die after a few days, without continued support from macrophages and DC activated cells will doe off)

44
Q

Direct anergy

A

Apoptosis and by molecular inhibition of immune functions (activated T cells are inherently pro apoptotic) •Tim-3
•PD1/ PD1L
•CTLA-4
All deactivate the immune response

45
Q

CTLA4-B7 binding

A

Makes less B7 molecules available for interaction with CD28; CTLA:B7 binding represses activation and block CD28 signalling (repression will shut down immune response)

46
Q

What does the lack of co-receptor signals mean

A

Anergy/death or compartmentalization

47
Q

T reg cells

A

T cells that regulate activation of other T cells and necessary to maintain peripheral tolerance to self antigens; Produce cytokines that shut down the immune system

48
Q

Natural T ref (nTreg)

A

Turn down immune response to self antigens

49
Q

Inducible or adaptive Treg cells

A

Generated to self and foreign antigen after an inflammatory immune response

50
Q

Hypersensitivity reactions

A

Allergy (Environment) and Autoimmunity (Self)

51
Q

Types of hypersensitivity reactions

A
  • Type I: Allergy (immediate)
  • Type II: Cytotoxic
  • Type III: Immune complex
  • Type IV: Delayed hypersensitivity or cell-mediated hypersensitivity
52
Q

Allergy response

A

IgE loading on mast cells, basophils, and eosinophils (mild reaction; rash, itching, swelling)

53
Q

Allergy treatment

A

Environmental control, antihistamines, steroids, leukotriene inhibitors, allergen immunotherapy. Antihistamine drugs often relieve many allergic symptoms; histamine is one of the mediators released from IgE-coated cells

54
Q

Anaphylaxis

A

Hypersensitivity reaction that may be life-threatening (fall in blood pressure and severe respiratory distress); Systemic response: peanuts, Bee sting, penicillin allergy
Require epinephrine to treat

55
Q

Biphasic anaphylaxis reaction

A

Have a less severe initial reaction and 24hrs later have a much worse one

56
Q

Atopic person

A

Allergy prone individual

57
Q

Environmental susceptibility

A

Hygiene hypothesis (overly clean can make you more susceptible to illness)

58
Q

Type 2: Cytotoxic

A

Antibody dependent (IgM, IgG) that combine with tissue or cell antigen creating lysis of cell or other membrane damage (examples: Autoimmune hemolytic anemia, blood transfusion reactions, Rh hemolytic disease, autoimmune glomerulonephritis)

59
Q

Type 3: Immune complex

A

Ag-Ab immune complexes deposited in tissues activate complement pathway; Neutrophils attracted to site, causing tissue damage (examples: Rheumatoid arthritis, systemic lupus erythematosus (SLE), some types of glomerulonephritis)

60
Q

Type 4: Cell-mediated, delayed hypersensitivity

A

Typically after 24-48 hours T lymphocytes are sensitized and activated on second contact with same antigen which induces inflammation and activates macrophages through lymphokines (Example: contact dermatitis, Diabetes Mellitus (T1), Rheumatoid arthritis)

61
Q

Treatment for autoimmune disease

A

Various immune suppressing drugs/therapies (Corticosteroids, cytotoxic drugs, NSAIDS, immunotherapy with various biologics, antibody treatments (monoclonal – blocking or IVIG), symptomatic)

62
Q

When can autoimmunity occur?

A

-Individual express MHC molecules that efficiently present self peptides (Two particular types of MHCII increase chance of type1 diabetes by 20 fold)
-Production of T and/or B cells that have receptors that recognize self (Random mix match, even identical twins will not share TCR repertoires (chance))
-Breakdown of tolerance mechanisms designed to eliminate these cells

63
Q

Potential causes of Autoimmunity

A

•Defects in central tolerance deletion/ survival
•Defects in T Reg function/ numbers
•Defective apoptosis mechanisms (+ve/-ve)
•Inadequate inhibitory receptor functions (CTLA/ Fas) •Chronic activation of APC’s, excessive T cell activation

64
Q

Autoimmunity development

A
  1. Genetic susceptibility
  2. Failure of self tolerance/immune control
  3. Infection/ injury
  4. Activation of APC’s
  5. Recruitment of auto-reactive
    lymphocytes
  6. Activation of auto-reactive Lymphocytes
  7. Tissue injury from auto immune attacks
  8. Auto immune disease
65
Q

Insulin dependent diabetes mellitus

A

Immune system targets insulin producing Beta cells in the pancreas (Islets of Langerhans) which is mediated by CTL activity, Dysfunctional natural Treg cells.

66
Q

Myasthenia Gravis

A

Self reactive antibodies bind to acetylcholine receptors which results in muscle weakness and paralysis

67
Q

Multiple Sclerosis

A

CNS inflammatory disease that is initiated by reactive T cells/ Macrophages causing chronic inflammation destroys myelin sheath protein, causing defect in sensory inputs

68
Q

Rheumatoid Arthritis

A

Systemic autoimmune disease; Cartilage protein targeted causing chronic joint inflammation (IgM, IgG antibody complexes form in joints)

69
Q

Lupus Erythematosus

A

Systemic: rash (forehead/ cheeks), inflammation of lungs, kidneys, joints, paralysis, convulsions; Breakdown in both T an B cell tolerance (lack of activation cell death may play a role)

70
Q

Genetic mutations associated with Autoimmune disorders include dysregulation of

A

-Treg (FoxP3)
-Cell activation (IL-2, IL-12, CD2/58, Blk)
-Activation inhibitors (IL-10, CTLA4)
-Apoptosis (Bim, Fas)
-HLA alleles (MHC)

71
Q

Which gender usually has an autoimmune disease

A

Women (80%), when makes get it they’re more severe

72
Q

Autoimmune treatment

A

Symptomatic/ Immunosuppression Drugs:
-Corticosteroids/anti-inflammatory
-Chemical T cell/ B cell inhibitors/Cytokine blockers (IL-2)
-mAb to block immune receptors on T/B cells or cytokines (TNFa)
-Pain control/physical therapy
-IVIG – block Fc receptors on cells

HSS 3305 (21 decks)

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