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Pathology > Disease of the Immune Systems > Flashcards

Disease of the Immune Systems Flashcards

1
Q

Three types of Failure of the Immune System:

A
  • Hypersensitivity (overactive immune syst)
  • Autoimmunity (recognition of self-antigens)
  • Immunodeficiency (ineffective immune syste)
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2
Q

Hypersensitivity type I:

A
  • Immediate, rapid response and mediated by mast cell degranulation. (Allergic reaction)
  • Result from the activation of the TH2 (subset of CD4+) by environmental antigens –> (class switching of B cell) production of IgE antibody –> release of vasoactive amines and other mediators from mast cells
  • Later: recruitment of inflammatory cells (neutrophils and T cells)
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3
Q

Hypersensitivity type II:

A
  • Antibody-mediated
  • Production of IgG, IgM that bind to antigen on target cell/tissue. Cause phagocytosis or lysis of target cell by the activation of complement or Fc receptors (recruitment of leukocytes) –> trigger pathological inflammation/ functional derangements (disturb the normal function of receptors or stimulate cellular responses excessively)
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4
Q

Hypersensitivity type III:

A
  • Immune complex-mediated.
  • Cause by antibodies binding to antigens to form complexes (deposited on tissue, in vascular beds –> Complement activation –> recruitment of leukocytes (neutrophils) by complement products and Fc receptors –> degranulation and release of enzymes (proteases) and toxic molecules –> stimulate inflammation –> tissue injury.
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5
Q

Hypersensitivity type IV:

A
  • Cell-mediated (Non-antibody mediated)
  • Delayed-type
  • Activate Th1 and Th17 (T cells) against self-antigen: 1. CD4+ T cells activated, release of cytokines, inflammation and macrophage. 2. CD8+ T cell-mediated cytotoxicity, releasing granzymes and others mediators.
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6
Q

Mast cells have high-affinity receptor for:

A
  • IgE antibodies (Fc epsilon receptors)

- Mast cells are ‘‘sensitized’’ to react if the antigen binds to the antibody molecules

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7
Q

IL-4 makes B cells undergo:

A

Class switching

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8
Q

Bronchial Asthma:

A

-Due to repeated exposure to antigen, there is a massive tissues remodeling (hypertrophy of the smooth muscles cells and fibrosis around the alveoli)

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9
Q

Systemic reactions (Anaphylactic shock):

A

Massive mast cell degranulation

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10
Q

Th1 and Th2 phenotype are 2 subcategories of T helper cells, factor favoring Th1:

A

presence of older siblings, early exposure to daycare, tuberculosis

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11
Q

Factor favoring Th2:

A

Only child, widespread use of antibiotics, western lifestyle, urban environment.

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12
Q

Hygiene hypothesis:

A

From birth we are primed into a Th-2 profile, but after repeated exposure to stimuli, our T cells develop a profile that is more Th-1.

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13
Q

Grave’s disease, there is antibodies that recognize thyroid stimulating hormone receptor. This trigger the receptor, causing the thyroid epithelial cells to produce thyroid hormones, leading to hyperthyroidism. Which type of Hypersensitivity is it?

A

Hypersensitivity type II. Immune complex formation at the surface of the cells (stimulates receptor without hormone)

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14
Q

Myasthenia gravis, is mediated by antibodies that couple to the acetylcholine receptor at the neuromuscular junction and cause muscle deficiencies. Which type of Hypersensitivity is it?

A

Hypersensitivity type II. The immune complex formation blocks the receptor function.

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15
Q

Blood transfusion reaction: if you are type A+ and you are receiving blood from a donor who has B- blood, which type of hypersensitivity?

A

Hypersensitivity type II. Pre-formed antibodies (that we have) will bind to B antigens on the RBCs which cause complement activation, causing lyse.

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16
Q

Newborn hemolytic anemia, reaction from the mother (Rh-) at the 2e exposure (baby delivery) to Rh+ antigens, memory B cells will target the Rh+ blood cells from the baby and attack it. Which type of hypersensitivity is it?

A

Hypersensitivity type II. The immune complex formation cause phagocytosis from complement activation.

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17
Q

Acute serum sickness, is the prototype of a systemic immune complex disease, 5 days after the foreign protein are inside the body, specific antibodies are produced and form antigen complexes in the circulation and deposit. Which type of hypersensitivity is it?

A

Hypersensitivity type III. Complexes deposit in the blood vessels in various tissue beds, triggering the subsequent injurious inflammation reaction.

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18
Q

Contact dermatitis due to poison ivy, urushiol become antigenic by binding to the host protein. On reexposure, sensitized TH1 CD4+ cells (memory T cells) accumulate in the dermis and migrate toward the antigen within the epidermis. Releasing cytokines leading to macrophages recruitment and others cytotoxic T cells that damage skin. Which type of hypersensitivity is it?

A

Hypersensitivity Type IV. T cells mediated and not antibodies.

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19
Q

Prolonged type IV hypersensitivity is characterized by:

A
  • T cells are replaced by macrophages, become large, flat, and eosinophilic (epithelioid cells)
    1. The epithelioid cells can fuse under the influence of cytokines (release of IFN-gamma) to form multinucleated giant cells.
    2. Aggregation of epithelioid cells (surrounded by a collar of lymphocytes) form Granulomas.
  • Can develop enclosing rim of fibroblasts and connective tissue.
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20
Q

Type I diabetes (islets), the immune system attack the beta cells in the pancreas (cells that secrete insulin) CD8+ T cell attacking the beta cells. Which type of hypersensibility is it?

A

hypersensitivity type IV. CD8+ T-cell mediated and not antibodies. Recognize target cells and kill them through the release of granzymes and perforins (holes to cause apoptosis)

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21
Q

Graft rejection is an example of which hypersensitivity?

A

Hypersensitivity type IV. CD8+ cell attacking the graft (release granzymes and perforins (holes to cause apoptosis)

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22
Q

Autoimmune diseases are due to:

A
  • Self-reactive T and B cells (Defective tolerance)

- Self-reactive T and B cells are normally eliminated (some T and B cells self-reactive escape).

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23
Q

Genes associated with Autoimmune Diseases?

A
  • Antigen recognition (HLA)
  • Immune cell signaling (PTPN22)
  • Inhibitory cytokines
  • Autophagy
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24
Q

Immune cell signaling (PTPN22) role:

A

Tyrosine phosphatase help self-reactive T cells to become activated. (suppresses immune signaling in lymphocytes)

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25
Q

Environmental triggers autoimmune diseases due to:

A
  1. Induction of costimulators on APCs by infections (more likely the T cell will become activated) More likely to attack our normal cells.
  2. Molecular mimicry of the normal cell from the antigens (close structure form our self-antigen) more likely to attack our normal cells.
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26
Q

Systemic Lupus Erythematosis symptoms:

A 
Butterfly rash
Hair loss
swollen joint
light sensitivity
glomerulonephrititis (hypersensitivity type III)
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27
Q

Lupus one of the classic feature of this disease is:

A

FAILURE TO MAINTAIN SELF-TOLERANCE: Production of a large number of autoantibodies directed against a lot of nuclear components (dsDNA, RNA, phospholipids)

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28
Q

Development of the Lupus (stages):

A
  1. Environment trigger causing tissue damage–>produce apoptotic cells
  2. Phagocytic clearance failure of apoptosis –> (DAMPs failure) defective clearance of NETs
  3. Lead to the production of autoantibodies. (antinuclear antibodies)
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29
Q

Production of autoantibodies in Lupus patient:

A

Defects in clearance and then the necrotic cells will undergo secondary necrosis (cell start to autolysis and release internal products) –> autoantibodies formation ( due to genetic susceptibility)

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30
Q

Due to secondary necrosis, Lupus may lead also to?

A

Type II hypersensitivity. (recognize antigens at the surface, destruction of RBC, platelets, neutrophils, lymphocytes..)

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31
Q

Gene involves in Rheumatoid Arthritis:

A 
HLA
Immune signaling (coreceptors)
Peptidylarginine deiminase (PADs)
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32
Q

Environmental factors trigger modification of host proteins:

A
  • Conversion of arginine to citrulline (citrullination) modulated by PADs (peptidylarginine deiminases) –> convert amine groups on the arginine residues to ketone groups
  • Immune system notice the abnormality and develop antibodies (anti-citrullinated protein ab)
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33
Q

Rheumatoid factors:

A

antibodies that recognize the Fc constant portion of IgG (characteristic of Rheumatoid arthritis)

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34
Q

Difference between osteoarthritis and rheumatoid arthritis?

A

Osteoarthritis involves erosion of the cartilage layer VS

Rheumatoid arthritis is an inflammatory disease (inflammation of the synovial membrane of these joints)

35
Q

Rheumatoid arthritis inflammation of the synovial membrane of the joints:

A
  • Hyperplasia of the synovial cells (vilification of the synovial membrane)
  • Massive infiltration underneath the synovial cells by the immune cells.
  • Cause erosion of the cartilage and bone.
36
Q

The infiltration of immune cells and hyperplasia of the synovial cells is called:

A

Pannus

37
Q

Inflammatory mediators in RA:

A

INF-gamma (Th1)
IL-17 (Th17)
TNF and IL-1 (macrophages)
RANKL (expressed on T-cells)

38
Q

RANKL involve in RA:

A

RANK ligand triggers excess differentiation into osteoclasts, resulting in more bone resorption. (RANKL instruct pre-osteoclast to fully become/ differentiate into osteoclasts)

39
Q

Multiple Sclerosis affects?

A

the myelin sheath in the CNS

40
Q

How is the immune cells manage to cross the BBB (normally cannot enter) in the MS:

A

Immune cells express the right combination of integrins, able to interact with the endothelial cells at the BBB and allow them to attach more firmly to enter the brain tissue.

41
Q

What happens when the immune cells enter the BBB in the MS:

A

Cells in the CNS encounter antigens that the immune systems never seen before and react to them (T cells and B cells triggering MS)

42
Q

Causes possible in MS:

A

Viral infections
HLA-DR2
Vit D deficiency???

43
Q

What can we see on the MRI scans to detect MS:

A

discoloration of the white matter in the brain.

44
Q

Relapsing-remitting MS (RRMS):

A

-Unpredictable attacks followed by periods of remission(small regeneration)

45
Q

Primary progressive MS (PPMS):

A

-Steady increase in disability without attacks

46
Q

Secondary progressive MS (SPMS):

A

Initial relapsing-remitting MS begins with decline without periods of remission.

47
Q

Progressive-relapsing MS (PRMS):

A

Steady decline since onset with super-imposed attacks.

48
Q

Crohn’s disease:

  1. Region affected
  2. Layer affected
  3. Morphology
A
  1. GI tract
  2. penetrating into muscle layer
  3. Transmural fissures, cobblestone appearance, Granuloma
49
Q

Ulcerative colitis:

  1. Region affected
  2. Layer affected
A
  1. Colon
  2. lesion restricted to mucosal layer
  3. Pseudo-polyps (regenerating ulcers), Crypt abscess (epithelial gland infiltrated with immune cells)
50
Q

T cell associated with different T cells.

  1. Crohn’s disease:
  2. UC:
A
  1. Th1

2. Th2

51
Q

Microbiome related to Crohn’s disease:

A
  • Reduced microbial diversity

- Specific strains overrepresented

52
Q

Genes involved in clearing infections related to Crohn’s disease:

A

NOD2 - PAMP receptor
ATG16L1 - autophagy
IL23R - proinflammatory
IRGM - autophagy

53
Q

NOD2, important gene associated with Crohn’s disease:

A
  • PAMPs released by microbes usually detected by NOD2 leading to signalling of NFkB.
  • Lack of signaling of NFkB, cause defects in barrier function, leading to inflammation, leakage, infiltration of these microbes, leading to chronic inflammation.
54
Q

Ulcerative colitis autoantibodies cause by:

A
  • Perinuclear anti-neutrophil cytoplasmic (pANCA) commun in this disease.
  • Molecular mimicry/cross-reactivity of host antibodies with certain bacteria and neutrophils.
55
Q

TH1 immunologic reaction triggered:

A

Macrophage activation
Stimulate IgG
Antibody production

56
Q

TH2 immunologic reaction triggered:

A

Stimulate IgE production

Activate mast cells and eosinophils

57
Q

TH17 immunologic reaction triggered:

A

Recruitment of neutrophils, monocytes.

58
Q

Lupus disease organ damage is mostly caused by:

A

Type III hypersensitivity.

59
Q

Transplant rejection is due to:

A

Mismatches in MHC causing the host immune cells to start attacking the graft (allograft).

60
Q

Direct alloantigen recognition:

A
  • T cells directly recognize the allogeneic (foreign) MHC molecules (cross-reaction).
  • Activate the host CD8+ T cells differenciate into CTLs, which kill the cells in the graft.
  • Host CD4+ helper T cells trigger into proliferation and cytokine production by recognition of donor class II MHC molecules and drive an inflammatiory response.
61
Q

Indirect alloantigen recognition:

A
  • Host CD4+ T cells recognize donor MHC molecules after the uptake, processing and presenting allogenic MHC molecules by recipient APC.
  • (same reaction than with other foreign antigens–>microbial) Secrete cytokines that induce inflammation and damage the graft.
  • Production of antibodies against graft alloantigens.
62
Q

Even complete matching of MHC genes does not ensure graft survival due to:

A

MHC produce proteins that are highly polymorphic and can be recognized by the immune system as being foreign.

63
Q

Hyperacute rejection

A
  • Type II hypersensitivity (preformed antidonor antibodies bind to graft endothelium immediately) or Blood incompatibility
  • Cause thrombosis and occlusion/ischemia of graft vessels
64
Q

Acute cellular rejection

A

-T cells destroy graft parenchyma (and vessels) by cytotoxicity and inflammatory reactions. CD4+ T cells (type IV hypersensitivity) recruiting macrophages and neutrophils that cause damage,

65
Q

Acute humoral rejection

A

Antibodies mediated; antibodies form within the capillaries induce complement activation (type II hypersensitivity reaction) induce inflammation, infiltration of immune cells in blood vessels.

66
Q

Chronic rejection

A

Dominated by arteriosclerosis, caused by T cell reaction and secretion of cytokines.

  • induce proliferation of vascular smooth muscles cells (hyperplasia)
  • associated with parenchymal fibrosis (due to occlusion of the blood vessels)
67
Q

Graft attacks host:

A
  • Graft vs Host disease (GVHD) occurs when immunocompetent tissue is transplanted into an immunocompromised host. (T cell recognize the host MHC molecules as non-self and attack)
  • Induction of co-stimulatory molecules of APC (host) due to the inflammatory environment.
  • Lead to production of costimulatory molecules (activation of T cells from the donor)
  • T cells of donor activated and engaged with cytokine profiles, attacking different tissues in the gut and hepatocytes in the liver.
68
Q

Primary (congenital) immune deficiencies:

A

faulty genes

  • Specific (antibody deficiencies, cell-mediated) involve mutations in genes compromising the immune system.
  • non-specific (complement defect, dysregulation or neutrophils defect)
69
Q

Secondary (acquire) immune deficiencies:

A

infections, cancer, immunosuppression drugs or aging and malnutrition.

70
Q

X-linked severe combined immunodeficiencies (X-linked SCID):

A
  • Mutation in gamma chains (cytokines receptor)

- No gamma chain, no maturation of T cell (stay immature)

71
Q

X-linked gamma globulinemia (BTK):

A

Tyrosine kinase defect involved in sending signal to the
proper maturation of B cells.
-No antibody production.

72
Q

AIDS causes by:

A

HIV

73
Q

Structure of HIV:

A
  • Nuclear capsid (with 2 copies of retroviral RNA genome and a reverse transcriptase)
  • Envelopped by the matrix
  • GP120 glycoprotein and GP41 (important feature of HIV to tropism and to enter into the cell)
74
Q

HIV affect:

A 
T cells (viral particule increase, T cells dies)
Macrophages and dendritic cells (reservoir for the virus)
75
Q

HIV entering in the cell steps:

A
  • Entry of HIV into cells requires the CD4 molecule, which acts as a high-affinity receptor for the virus.
  • HIV enveloppe need also to bind to others surface molecule (coreceptor) –> Chemokine receptors CCR5 and CXCR4
  • Conformational change
  • Allow gp120 to associate with other receptors.
76
Q

Why the CCR5 and CXCR4 are critical components of the HIV infection?

A

because without it, HIV tropism and enter into the cell cannot be done.

77
Q

GP120 responsible to:

A

binds with chemokine receptor (CCR5 and CXCR4)

78
Q

GP41 responsible to:

A

Membrane penetration.

79
Q

HIV once is in the cell:

A
  • Reverse transcriptase (convert RNA into DNA)
  • T-cell receives cytokine signals, induce proliferation of the cells.
  • HIV RNA transcripts can be produced and repeat itself (structural core components of the virus) into the genome before its release.
80
Q

Why it is hard for the immune system to get ride of the virus?

A

The virus is highly mutagenic and escape the protection from the immune system. The immune system hard time to track the virus.

81
Q

Mechanism of T cell depletion:

A
  • Direct killing of CD4+ T cells (membrane permeability and protein synthesis –>cytopathic effect of virus)
  • CD4+ T cells recognized by CD8+ T cells that recognize this cell is infected and directly kill it.
  • Activation of uninfected CD4+ T cells undergo apoptosis (cell death)
82
Q

Course of an HIV infection:

A
  1. Death of mucosal CD4+ T cells
  2. Lymph nodes infected and spread out (viremia)
  3. Partial control of infections (production of antibodies and activation of cytotoxic T cells)
  4. Chronic stage (battle between HIV numbers and T cells numbers)
  5. Terminal stage (Progressive loss of T cell until natural immunity lost)
83
Q

Treatment available, but NO CURE:

A

Anti-retroviral therapy

Pathology (23 decks)

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