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Immunology (Part Two) > 21 – Autoimmunity and Immune Deficiencies > Flashcards

21 – Autoimmunity and Immune Deficiencies Flashcards

1
Q

Autoimmunity:

A

-inescapable hazard associated with acquired immunity
>also have the potential for immune self destruction
*develop spontaneously (predisposing causes are rarely obvious)

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2
Q

Autoimmune diseases are pathological condition(s) associated with:

A

-ongoing tissue damage from self-reactive antibodies and/or cytotoxic T cells

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3
Q

Autoimmune conditions are:

A

-failures of immune tolerance and immunoregulation
>normal regulatory mechanisms do not function to PREVENT or DOWN-REGULATE the response to self-antigens

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4
Q

What causes autoimmunity:

A
  1. Exposure of ‘hidden’ antigens
  2. New epitopes/antigens
  3. Cross-reactive antigens
  4. Bystander activation
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5
Q

Exposure of ‘hidden’ antigens:

A

-antigens not normally exposed to immune cells (ex. in eye, CNS) or exposure of previously ‘cryptic’ epitopes (usually hidden)
*normally protected from exposures so no active tolerance
*inflammation

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6
Q

Inflammation due to exposure of ‘hidden’ antigens:

A

-exposure of antigens leads to triggering of immune response and auto-immune disease

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7
Q

New epitopes/antigens:

A

-generated on self proteins by molecular changes
>Ex. IgG Fc after binding to antigen to creat an immune complex
*ex. rheumatoid factor

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8
Q

Rheumatoid factor:

A

-auto-antibodies to the Fc portion of IgG in immune complexes

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9
Q

Cross-reactive antigens:

A

*’molecular mimicry’
-immune responses to an infectious agent which shares epitopes to self-antigen
>body produces antigens against the infectious agent and the self-antigen
Ex. Rheumatic fever after Streptococcus infection

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10
Q

Rheumatic fever after Streptococcus infection:

A

-Streptococcus cell wall stimulates antibody response
-some antibodies will cross-react with heart valve tissue

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11
Q

Bystander activation:

A

-once immune response is triggered, APCs in area are activated and have enhanced interactions with Th cells
>high levels of cytokines supply the co-stimulatory signals needed to trigger self-reactive cells
*both bacteria and viruses have done this to induce auto-immunity

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12
Q

2 groups of autoimmune diseases:

A

*may share common mechanisms
1. Organ Specific AIDs
2. Systemic AIDs

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13
Q

organ-specific AIDs:

A

-selective targeting of a single organ or cell type (or related cells/organs)
*predominantly Th2 immune response

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14
Q

Systemic AIDs:

A

-auto-reactivity to multiple self antigens in unrelated tissues, cells, and organs
-many are intracellular (including components of nucleus)
-circulating immune complexes are important in pathogenesis of the lesions
*both Th1 and Th2 immune Reponses

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15
Q

Examples of organ-specific AID: endocrine

A

-hypothyroidism
-diabetes
-Addison’s disease (adrenal medulla

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16
Q

Examples of organ-specific AID: neurological

A

-polyneuritis
-meningitis
-myelopathy
-myasthenia gravis

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17
Q

Examples of organ-specific AID: others

A

-ocular: keratitis
-skin: pemphigus
-muscle: polymyositis
-joints: polyarthritis
-blood cells: rbcs, platelets

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18
Q

Systemic AID example:

A

systemic lupus erythematosus and related syndromes
>Sjogrens syndrome
>rheumatoid arthritis
>dermatomyositis

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19
Q

Systemic AID diseases in people are called:

A

-rheumatic or
-connective tissue or
-collagen diseases

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20
Q

Related systemic AIDs and symptoms often occur in:

A

-the same individuals and related individuals
-maybe due to the defects in ‘aire’
>lack of expression enables TCR recognizing those self-antigens to escape deletion

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21
Q

Autoimmune disease summary:

A

-rare
-usually maintained
-precise mechanisms not understood (maybe Aire gene)
-appear spontaneously and randomly
-few predisposing factors ID (genetics of MHC II important)
-vary in severity
-spontaneous exacerbations and remissions are common

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22
Q

Types of immune deficiencies:

A

-primary
-secondary

23
Q

Primary immune deficiencies:

A

-symptoms arise usually in young animals
>after maternal immunity wanes
Ex. leukocyte adhesion deficiency

24
Q

Secondary immune deficiencies:

A

-often induced by pathogens or toxic substances

25
Q

Points in the immune system development where blocks may lead to immunodeficiency:

A

-lymphoid precursors: combined ID
-neutrophils: neutrophil defects
-thymic processing: thymic aplasia
-‘bursal’ processing: agammaglobulinemia
-antibodies: deficiencies in individual Ig classes

26
Q

Signs of primary immune deficiency:

A

-increased susceptibility to infections at a young age
>pathogens
>opportunistic invaders

27
Q

Other (lesser) associations with primary immunodeficiency:

A

-increased IgE responses (allergy)
-increased autoimmune diseases
-increased malignancies

28
Q

Leukocyte adhesion deficiency:

A

-defect in adhesion proteins that enable neutrophils to leave the bloodstream and enter the tissues in response to chemotaxic factors

29
Q

Leukocyte adhesion deficiency: species

A

-Irish setters
-Holstein cattle (BLAD)
>affected cattle usually die at 2-7months
*autosomal recessive inheritance

30
Q

Leukocyte adhesion deficiency clinically:

A

-recurrent bacterial infections (particularly at mucosal surfaces)
-stunted growth
-fever
-persistent neutrophilia

31
Q

Canine and bovine leukocyte adhesion deficiency:

A

-deficiency in INTEGRIN molecules CD11b/CD18 found on neutrophil surfaces
-CD18 also involved in T cell adhesion and emigration from vessels so affected cattle have decreased DTH (delayed type hypersensitivity) responses

32
Q

Severe combined immunodeficiency (SCID) occurs in:

A

-people
-cattle
-dogs
*most commonly in horses (Arabs)

33
Q

SCID inherited as autosomal recessive:

A

-used to occur in 2-3% Arabs
-also in related horses (Appaloosa)
-introduced into NA by a single stallion in 1920s
*carrier status level of carriers is 8% so is now rare to see clinical cases

34
Q

What is SCID?

A

*no production of functional T or B cells (do have some NK cells)

35
Q

SCID diagnosis:

A

-can’t palpate lymph nodes
-very low numbers of circulating lymphocytes
-no IgM in presuckle serum

36
Q

SCID clinically:

A

-survive for as long as colostral Ig (a few weeks)
-die from first opportunistic invader (often adenoviruses)

37
Q

Jack Russell Terriers and SCID:

A

-autosomal recessive
-estimated 1.1% carrier frequency
-IgG has a half life of about 3 weeks

38
Q

B cell defects:

A

-lower levels of serum Igs
*agammaglobinemia: no B cells, no serum Igs

39
Q

Agammaglobinemia:

A

-rare disease of foals
-lymphoid tissues have no germinal centers
-recurrent bacterial infections
-usually survive a few weeks (until colostral protection wanes)

40
Q

Selective IgA deficiency dog breeds:

A

-german shepherds (low IgA)
-beagle
-English cockers

41
Q

Selective IgA deficiency:

A

-infections at ‘surfaces’
>respiratory, skin, eyes
-low IgA associated with range of infections at skin and GI tract
>deep pyoderma
>small intestine bacterial growth (SIBO)

42
Q

T cell defects:

A

-incompatible with life, so fewer conditions
-since no T cell help, the B cell responses are minimal
Ex. ‘nude defect’

43
Q

‘nude defect’:

A

-congenital hypotrichosis and thymic aplasia
-cats, rats, pigs, calves, guinea pigs, mice
*no thymus: no T cell development
-defect in epithelial cells of the thymus and of skin=hairless

44
Q

Secondary immune defects types:

A

-pathogen induced
-other agents and conditions
-drugs

45
Q

Infectious bursal disease virus in chickens: (primary lymphoid tissue)

A

-affects bursa (site of primary B cell development)
-affects B cell areas in secondary lymphoid organs
*infections in hatchlings result in B cell destruction and inability to make antibodies
>in older birds, the effects are less dramatic than in young

46
Q

Primate retroviruses symptoms: (secondary lymphoid tissues)

A

-decrease in CD4+ T cells
>virus entry into cells is by adhesion to CD4 molecule
-destruction of CD4 cells results in failure of Ab response and cell mediated immunology
-deaths associated with opportunistic infections
Ex. HIV

47
Q

Feline immunodeficiency virus (FIV) infects: (secondary lymphoid tissues)

A

-T cells
-megakaryocytes
-macrophages
-dendritic cells
-neuronal cells
*all T cells are decreased (decrease in CD4 to CD8 ratio)

48
Q

FIV clinical syndrome:

A

-develops over many years
>associated with both lymphoid follicular hyperplasia then gradual depletion of T cells
*cats succumb to bacterial infections, wasting

49
Q

Canine Distemper Virus, CDV (secondary lymphoid organs)

A

-infects and destroys secondary lymphoid organs
-depresses activities of lymphocytes and macrophages (decrease IL-1 and IL-2 production)
-deaths from secondary infections or nervous system inflammation

50
Q

Examples of viruses that infect and destroy ALL rapidly dividing cells: (secondary lymphoid organs)

A

-will infect and destroy cells in GERMINAL CENTERS
-Feline panleukopenia virus
-canine parvovirus
-african swine fever virus

51
Q

Corticosteroids can affect:

A

-leukocyte circulation
-immune effector mechanism
-modulate inflammatory mediators actions

52
Q

Corticosteroids affects leukocyte circulation:

A

-usually lymphopenia and neutrophilia
>reduced emigration of neutrophils into tissues

53
Q

Corticosteroids affect on immune effector mechanisms:

A

-decreased chemotaxis and phagocytosis
-decreased cytokine production (decreasing T cell responses)

54
Q

Corticosteroids affect on modulate inflammatory mediator actions:

A

-inhibit the acute inflammatory response
>decreased macrophage production of prostaglandins and IL-1

Immunology (Part Two) (18 decks)

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