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Mandal > Immune Tolerance and Autoimmune Disease > Flashcards

Immune Tolerance and Autoimmune Disease Flashcards

1
Q

Normally microbes are _____ and self antigens are _____

A

immunogenic, tolerogenic

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2
Q

Normal immune response +microbe=

A

proliferation and differentiation

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3
Q

Self-tolerance + self antigen =

A
  • Anergy- functional unresponsiveness
  • Deletion- Cell death
  • Change in specificity- receptor editing
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4
Q

Immune Tolerance

A
  • Tolerance is a lack of response to an antigen that is induced by previous exposure of lymphocytes
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5
Q

Normal indiv are tolerant to

A

self Antigens

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6
Q

failure of self-tolerance results in

A

autoimmunity

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7
Q

immune tolerance can be use therapeutic for

A
  • Organ transplantaion
  • Autoimmune disease
  • Allergic diseases
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8
Q

Central tolerance

A
  • Immunological tolerance to self antnigens induced in immature lymphocytes in bone marrow and thymus
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9
Q

central tolerance mechanisms

A
  • Deletion ( cell death)
  • Receptor editing (change in BCR)
  • Devlopment of TRegs
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10
Q

deficiency of ____ shown in many autoimmune diseases in humans

A

TRegs

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11
Q

Central tolerance for T lymphocytes

Positive selection in Thymus

A
  • low-affinity interaction of TCR with self MHC molecule positively selects and rescues thymocytes from programmed cell death
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12
Q

Central tolerance for T lymphocytes

negative selection in Thymus

A

apoptoic death

deletion of self-reactive t cells devlops central tolerance

(prevents future autoimmune diseases)

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13
Q

Perpheral Tolerance

A
  • Immune tolerance to self antigens in peripheral tissues encounterd by mature lymphocytes
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14
Q

Peripheral Tolerance Mechanisms

A
  • Clonal Anergy: (B7:CD28)
  • Deletion: cell death
  • Suppression via
    • Tregs
    • Il-10
    • TGF-Beta
    • block macrophage activation
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15
Q

Mucosal Tolerance

3 independent mechanisms

A
  • Ignorance
    • of antigen by the immune system (anergy)
  • Deletion
    • of T cells
  • Generation of regulatory T cells
    • controls inflammatory response
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16
Q

Safeguard against autoimmunity

A
  • Tolerance to self Ag is learned/acquired
  • lymphocytes recognize self-Ag and become autoreactive
  • autoreactive lymphocytes absent due to central and peropheral tolerance
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17
Q

Autoimmune Diseases

A
  • failure of self-tolerance
  • adaptive immune responses against self antigens
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18
Q

autoimmune diseases genteic factors

A

HLA association

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19
Q

Autoimmune disease generation of

A
  • autoreactive B cells
  • autoreactive T cells
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20
Q

auto-abs or autoreactive T cells attack

A

body’s own cells, tissues and organs

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21
Q

attack on the body’s own cells, tissue, and organs causing

A

inflammation and tissue damage through

  • Hypersensitivity reactions II, III, IV
  • Compliment activation
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22
Q

autoimmune diseases are

A

very common, often chronic and long lasting

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23
Q

complement activation leads to

(autoimmune disease development )

A
  • inflammaiton
  • deficiency in complement proteins (C1q, C2, C4)
  • Result: no clearance of immune complexes & apoptotic cells
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24
Q

Antibody-dependent cytotoxic

Hypersensitivity (Type II)

A
  • Ag-Ab binding activates cytotoxic cells, killing antigenic target cells

(Type II- IgM and IgG Abs binding to Ags)

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25
Q

Three mechanisms for Type II cytotoxicity

A
  1. Lysis of cells
  2. Cell injury by inflammatory cells
  3. Phagocytosis of antobody coated cells
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26
Q

Immune complex-mediated hypersensitivity

(type III)

A
  • inflammation
  • Immune complex deposition-mediated diseases
  • immune complex formation in blood vessels:
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27
Q

immune complex formation despositon in blood vessels triggers

(type III)

A
  • Platelet aggregation
  • complement activation
  • microthrombi formation
  • C5a C3a recruitment of PMNs
    • damage to the blood vessel
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28
Q

type(IV)/DTH

A
  • T cell mediated inflammatory response
  • antigen-specific TH1-type CD4 T cells
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29
Q

type IV/ DTH ( delayed-type hypersensitivity) diseases

A
  • Contact dermatitis (Haptens)
  • TB
  • Granulomas (TB and leprosy)
  • allergic reactions to pathogens (bacteria, viruses, fungi)
  • Rejection of transplants
  • Autoimmune disease
30
Q

type II hypersensituvity Ab-induced damage

A
  • idiopathic thrombocytopenic purpura
  • autoimmune hemolytic anaemia
31
Q

type II hypersensitivity

Ab-induced receptor stimulation or blockade

A
  • Grave’s disease
  • Myasthenia gravis
  • Insulin receptor Ab syndrome
32
Q

type III hypersensitivity

A

systemic lupus erythematosus

Vasculitis

33
Q

type IV hypersensitivity

A
  • Insulin-dependent diabetes mellitus
  • Hasimoto’s thyroiditis
  • Rheumatoid arthritis
  • Multiple Sclerosis
34
Q

Anti- DNA antibody associated with which diseas ?

A

Lupus n

35
Q

Complement-fixing autoantibodies associated with which autoimmune diseases

A

autoimmune anemias

thrombocytopenia

36
Q
A
37
Q

tissue-specific autoantibodies associted with which diseases

A

systemic Lupus Erythematosus (SLE)

Rheumatoid arthritis (RA)

Type I Diabetes mellitus

38
Q

autoantibodies to cell-surface receptors associated with which diseases

A

grave’s disease

myasthenia gravis

39
Q

Autoimmune hemolytic anemia

target antigen

mechanisms of disease

clinical manifestations

A
  • RBC membrane proteins (Rh Ag)
  • opsonizaton and phagocytosis of erythrocytes
  • Hemoylsis anemia
40
Q

Autoimmune thrombocytopenic purpura

target antigen

mechanisms of disease

clinical manifestations

A
  • platelet membrane proteins
  • opsonization and phagocytosis of platelts
  • Bleeding
41
Q

Acute rheumatic fever

target antigen

mechanisms of disease

clinical manifestations

A
  • Streptococcal Ag specific Ab crossreacts myocardial Ag
  • inflammation macrophage activation
  • Myocarditis, Arthritis
42
Q

myasthenia gravis

target antigen

mechanisms of disease

clinical manifestations

A
  • Acetylcholline (Ach) receptor
  • Antibody inhibits Ach binding
  • muscle weakness and paralysis
43
Q

Graves’ disease

target antigen

mechanisms of disease

clinical manifestations

A
  • TSH (thyroid stimulating hormone) receptor
  • Ab-mediated stimulation of TSH receptors
  • Hyperthyroidism
44
Q

autoantibodies to receptors bind

A

to cell memebrane receptors and interfere with endogenous ligand binding to the receptor

45
Q

Patient with graves’ disease

A
  • hyperthyroidism
  • exophthalmos
  • Blood tests
    • overactive thryroid
    • autoantibodies to thyroid peroxidase
    • increase of T3 and T4 levels
46
Q

mechanisms of T cell-mediated tissue injury

A
  • self Ag activate T cells causing tissue injury and autoimmune disease
    *
47
Q

cell injury in type 1 diabetes, RA or MS is mediated by

A

Th cells via DTH

48
Q

cell killind mediated by

A

CTLs

49
Q

Tissue injury by

Killing of target cells by

A

Th cells

CTLs

50
Q

T cell-mediated autoimmune diseases list

A
  1. type 1 diabetes
  2. rheumatoid arthritis
  3. multiple sclerosis
  4. hasimoto’s thyroiditis
51
Q

type 1 diabetes

antigen

clinical manifestations

A
  • islet cell Ag
  • impaired glucose metabolism, vascular diseses
52
Q

rheumatoid arthritis

antigen

clinical manifestations

A
  • synovial fluid Ag
  • inflammation & erosion of joints & bones
53
Q

multiple sclerosis

antigen

clinical manifestations

A
  • myelin protein
  • demyelination of CNS, sensory and motor dysfunction
54
Q

hasimoto’s thyroiditis

antigen

clinical manifestations

A
  • thyroglobulin
  • destruction of thyroid gland, hypothyroidism
55
Q

Molecular Mimicry in rheumatic fever

A
  • leads to inflammatory disease of the heart valves
  • carbohydrate Antigens on the group A streptococcal cell wall cross- react with a heart valve Atigens
56
Q

Diseases of molecular mimicry

autoimmune disease

A
  • rheumatic
  • type I diabetes
  • Guillain-Barre syndrome
57
Q

link btwn RA and ______established through____

A

periodonitis, protein citrullinatoin

58
Q

P.gingivalis infection and autoimmune disease due to

A
  • heat shock proteins (HSP) 60 from P. gingivalis
  • causes periodontitis & autoimmune atherosclerosis
    • Genteic factors
    • inflammation
    • TNF-alpha production
59
Q

treatment of P.gingivalis infection in RA patients

A
  • anti-TNF-alpha treatment
    • Infliximab
    • Remicade
    • Humira
  • Omega-3 fatty acids
    • reduces swelling, helps tender joints
  • Dietary polyphenols
60
Q

How does an autoimmune disease develop?

A
  • not fully understood
  • self-Ag is not expressed in the thyms
  • genic predisposition
61
Q

Diagnosis of autoimmune diseases

A
  • tissue biopsies
    • Ab
    • complement proteins
  • determination of auto-Ab
62
Q

treatment of autoimmune diseases

that block inflammation

A
  • NSAIDS
  • COX-2 inhibitors
  • Corticosteroids
63
Q

treatment of autoimmune diseases

cyclophosphamide

A

prevents proliferation B cells

(reduces auto-Ab production used in SLE)

64
Q

treatment of autoimmune diseases

Infliximab (Remicade)

Adalimumab(Humira)

A
  • Anti-TNF- alpha mAb
  • control inflammation
  • used in crohn’s disease
  • RA
65
Q

treatment of autoimmune diseases

Rituximab

A
  • Anti-CD20 mAb
  • eliminates B cells used in RA SLE
66
Q

central tolerance

A
  • Apoptosis (deletion)
  • Receptor editing B cells
  • Development of regulatory T lymphocytes (CD4+ T cells only)
67
Q

Peripheral tolerance

A
  • Anergy
  • Apoptosis (deletion)
  • suppression
68
Q

Molecular Mimicry

A
  • presence of autoreactive B cells recognizes self-Ag and also cross-reactive to foreign Antigen
  • Cross-reactive foreign Antigen triggers Th cell activation and cytokine secretion
69
Q

Cross-reactive foreign Antigen triggers Th cell activation and cytokine secretion

A
  • B cell proliferate, differentiate, and secrete autoantibodies
  • The antibodies bind to the pathogenic structures and control infection
  • Residual auto-abs bind to self-Ag and may trigge autoimmune disease
70
Q

Therapeutic Applications of Mucosal Tolerance in Autoimmune Diseases

A
  • trails in patients with MS, RA, diabetes
  • T cell proliferative responses were affected and TGF-B secreting cells were present in treated patient

Mandal (7 decks)

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