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Pathology > Summary's Chapter 5: Diseases of the immune disease > Flashcards

Summary's Chapter 5: Diseases of the immune disease Flashcards

1
Q

Fill in: The innate immune system uses several families of receptors, such as the … receptors, to recognize molecules present in various types of microbes and produced by damaged cells.

A

Toll-like

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2
Q

Fill in: … are the mediators of adaptive immunity and the only cells that produce specific and diverse receptors for antigens.

A

Lymphocytes

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3
Q

Explain what T-lymphocytes express, how they are recognized and where

A

T (thymus-derived) lymphocytes express antigen receptors called T-cell receptors (TCRs) that recognize peptide fragments of protein antigens that are displayed by MHC molecules on the surface of antigen-presenting cells.

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4
Q

Explain what B-lymphocytes express, how they are recognized and where

A

B (bone marrow–derived) lymphocytes express membrane-bound antibodies that recognize a wide variety of antigens. B cells are activated to become plasma cells, which secrete antibodies.

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5
Q

What are Natural Killer cells?

A

Natural killer (NK) cells kill cells that are infected by some microbes, or are stressed and damaged beyond repair. NK cells express inhibitory receptors that recognize MHC molecules that are normally expressed on healthy cells, and are thus prevented from killing normal cells.

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6
Q

What do antigen-presenting cells (APCs) do?

A

Antigen-presenting cells (APCs) capture microbes and other antigens, transport them to lymphoid organs, and display them for recognition by lymphocytes. The most efficient APCs are DCs, which live in epithelia and most tissues.

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7
Q

How are the cells of the immune system oragnized?

A

The cells of the immune system are organized in tissues, some of which are the sites of production of mature lymphocytes (the generative lymphoid organs, the bone marrow, and thymus), and others are the sites of immune responses (the peripheral lymphoid organs, including lymph nodes, spleen, and mucosal lymphoid tissues).

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8
Q

What system is first activated in respons to a microbe?

A

The innate immune resopns

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9
Q

What are components of the innate immune response?

A

Epithelial barriers, phagocytes, NK cells, and plasma proteins, for example, of the complement system

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10
Q

Does the innate immune system have antigen specificity or memory?

A

No, the adaptive system has these properties

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11
Q

How are innate immune reactions often manifested?

A

As inflammation

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12
Q

How does the adaptive immune respons differ from the innate?

A

The defense reactions of adaptive immunity develop slowly, but are more potent and specialized.

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13
Q

What happens to microbes and other foreign antigens that are captured by DCs?

A

They are transported to lymph nodes, where the antigens are recognized by naïve lymphocytes. The lymphocytes are activated to proliferate and differentiate into effector and memory cells

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14
Q

Fill in: Cell-mediated immunity is the reaction of …, designed to combat cell-associated microbes (e.g., phagocytosed microbes and microbes in the cytoplasm of infected cells). Humoral immunity is mediated by … and is effective against extracellular microbes (in the circulation and mucosal lumens).

A

T lymphocytes, antibodies (respectively)

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15
Q

CD4+ helper T cells / CD8+ cytotoxic T lymphocytes* help B cells to make antibodies, activate macrophages to destroy ingested microbes, stimulate recruitment of leukocytes, and regulate all immune responses to protein antigens

A

CD4+ helper T cells

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16
Q

CD4+ helper T cells / CD8+ cytotoxic T lymphocytes kill cells that express antigens in the cytoplasm that are seen as foreign (e.g., virus-infected and tumor cells)

A

CD8+ cytotoxic T

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17
Q

The functions of CD4+ T cells / CD8+ T cells are mediated by secred proteins called cytokines

A

Both!

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18
Q

… secreted by plasma cells neutralize microbes and block their infectivity, and promote the phagocytosis and destruction of pathogens. … also confer passive immunity to neonates.

A

Antibodies

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19
Q

How is immediate (type 1) sensitivity also called?

A

Allergic reaction / allergy

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20
Q

How is type 1 hypersensitivity induced?

A

By environmental antigens (allergens) that stimulate strong TH2 responses and IgE production in genetically susceptible individuals.

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21
Q

How does IgE play a role in allergies?

A

IgE coats mast cells by binding to the FcεRI receptor; reexposure to the allergen leads to cross-linking of the IgE and FcεRI, activation of mast cells, and release of mediators.

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22
Q

What are principal mediators (including granule contents)?

A

Principal mediators are histamine, proteases, and other granule contents; prostaglandins and leukotrienes; and cytokines.

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23
Q

What is the role of mediators?

A

Mediators are responsible for the immediate vascular and smooth muscle reactions and the late-phase reaction (inflammation).

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24
Q

How can the clinical manifestations differ in hypersensitivity (type 1)?

A

The clinical manifestations may be local or systemic, and range from mildly annoying rhinitis to fatal anaphylaxis.

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25
Q

What is a synonym of coat

A

opsonize

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26
Q

What does coat/opsonize mean?

A

To increase the susceptibility of (bacteria/other foreign cells) to ingestion by phagocytes

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27
Q

How are pathogens opsonized? (explain the process)

A

Antibodies can coat (opsonize) cells, with or without complement proteins, and target these cells for phagocytosis by phagocytes (macrophages), which express receptors for the Fc tails of lgG and for complement proteins. The result is depletion of the opsonized cells.

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28
Q

Antibodies and immune complexes may deposit in tissues or blood vessels and elicit either of two reactions. Which two?

A
  • Acute inflammatory reaction by activating complement, with release of breakdown products
  • By engaging Fc receptors of leukocytes
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29
Q

Does the inflammatory reaction per definition cause tissue injury?

A

yes

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30
Q

How can antibodies attack foreign cells without cell injury

A

Antibodies can bind to cell surface receptors or other essential molecules and cause functional derangements (either inhibition or unregulated activation)

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31
Q

Explain how cytokine-mediated inflammation works

A

CD4+ T cells are activated by exposure to a protein antigen and differentiate into TH1 and TH17 effector cells. Subsequent exposure to the antigen results in the secretion of cytokines. IFN-γ activates macrophages to produce substances that cause tissue damage and promote fibrosis, and IL-17 and other cytokines recruit leukocytes, thus promoting inflammation.

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32
Q

How is classical T cell-mediated inflammatory reaction also called?

A

Delayed-type hypersensitivity

33
Q

Chronic TH1 reactions associated with macrophage activation often lead to …

A

granuloma formation

34
Q

Explain how T-cell mediated cytotoxicity works

A

CD8+ cytotoxic T lymphocytes (CTLs) specific for an antigen recognize cells expressing the target antigen and kill these cells. CD8+ T cells also secrete IFN-γ.

35
Q

What is tolerance (of self antigens)?

A

Unresponsivevness

36
Q

What is the breakdown of tolerance?

A

The basis of auto-immune diseases

37
Q

What are the two types of tolerances?

A

Central and peripheral tolerance

38
Q

Explain how central tolerance works

A

Immature T and B lymphocytes that recognize self antigens in the central (generative) lymphoid organs are killed by apoptosis; in the B-cell lineage, some of the self-reactive lymphocytes switch to new antigen receptors that are not self-reactive.

39
Q

Explain how peripheral tolerance works

A

Mature lymphocytes that recognize self antigens in peripheral tissues become functionally inactive (anergic), are suppressed by regulatory T lymphocytes, or die
by apoptosis.

40
Q

The factors that lead to failure of self-tolerance and the development of autoimmunity include two things. Which two?

A

(1) inheritance of susceptibility genes that disrupt different tolerance pathways, and (2) infections and tissue injury that expose self antigens and activate APCs and lymphocytes in the tissues.

41
Q

What is SLE (Systemic lupus erythematosus)?

A

SLE is a systemic autoimmune disease caused by autoantibodies produced against numerous self antigens and the formation of immune complexes.

42
Q

Fill in: The major autoantibodies, and the ones responsible for the formation of circulating immune complexes, are directed against … . Other autoantibodies react with red blood cells, platelets, and various phospholipid-proteins complexes.
(in regard to SLE)

A

nuclear antigens

43
Q

What are the disease manifestations of SLE?

A

Disease manifestations include nephritis, skin lesions, and arthritis (caused by the deposition of immune complexes), hematologic abnormalities (caused by antibodies against red cells, white cells and platelets) and neurologic abnormalities (caused by obscure mechanisms).

44
Q

What is the underlying cause of the breakdown of self-tolerance in SLE?

A

This is unknown

(non-exclusive possiblities include excessive generation or persistence of nuclear antigens, in individuals with inherited susceptibility genes, and environmental triggers (e.g., UV irradiation, which results in cellular apoptosis and release of nuclear antigens))

45
Q

What is the Sjögren syndrome?

A

Sjögren syndrome is an inflammatory disease that primarily affects the salivary and lacrimal glands, causing dryness of the mouth and eyes.

46
Q

What is the Sjögren syndrome caused by?

A

(it is believed to be caused) By an autoimmune T-cell reaction against an unknown self antigen expressed in these glands, or immune reactions against the antigens of a virus that infects the tissues.

47
Q

What is a synonym of systemic sclerosis?

A

scleroderma

48
Q

How is sytemic sclerosis characterized?

A

By progressive fibrosis involving the skin, gastrointestinal tract, and other tissues.

49
Q

What may fibrosis be the result of? (in systemic sclerosis)

A

Fibrosis may be the result of activation of fibroblasts by cytokines produced by T cells, but what triggers T cell responses is unknown.

50
Q

What clinical manifestations are often seen in systemic sclerosis? And what is the pathogenesis of these manifestations?

A

Endothelial injury and microvascular disease are commonly present in the lesions of systemic sclerosis, perhaps causing chronic ischemia, but the pathogenesis of vascular injury is not known.

51
Q

Rejection of solid organ transplants is initiated mainly by …

A

host T cells that recognize the foreign HLA antigens of the graft

52
Q

In which two ways can a host T cell recognize a foreign HLA antigen of the graft? (and explain the cells involved)

A

directly (on APCs in the graft) or indirectly (after uptake and presentation by host APCs)

53
Q

There are different types and mechansims of rejection of solid organ grafts. What are these 4 types?

A
  • Hyperacute rejection
  • Acute cellular rejection
  • Acute antibody-mediated (humoral) rejection
  • Chronic rejection
54
Q

Explain hyperacute rejection

A

Preformed anti-donor antibodies bind to graft endothelium immediately after transplantation, leading to thrombosis, ischemic damage, and rapid graft failure.

55
Q

Explain acute cellular rejection

A

T cells destroy graft parenchyma (and vessels) by cytotoxicity and inflammatory reactions.

56
Q

Explain acute antibody–mediated (humoral) rejection

A

Antibodies damage graft vasculature.

57
Q

Explain chronic rejection

A

Dominated by arteriosclerosis, this type is caused by T cell activation and antibodies. The T cells may secrete cytokines that induce proliferation of vascular smooth muscle cells, and the antibodies cause endothelial injury. The vascular lesions and T cell reactions cause parenchymal fibrosis.

58
Q

(This questions is for overview purpose, so you can clearly see the differences)
What are the different types and mechanisms of rejections of a graft?

A
  • Hyperacute rejection: Preformed anti-donor antibodies bind to graft endothelium immediately after transplantation, leading to thrombosis, ischemic damage, and rapid graft failure.
  • Acute cellular rejection: T cells destroy graft parenchyma (and vessels) by cytotoxicity and inflammatory reactions.
  • Acuteantibody-mediated (humoral) rejection: Antibodies damage graft vasculature.
  • Chronic rejection: Dominated by arteriosclerosis, this type is caused by T cell activation and antibodies. The T cells may secrete cytokines that induce proliferation of vascular smooth muscle cells, and the antibodies cause endothelial injury. The vascular lesions and T cell reactions cause parenchymal fibrosis.
59
Q

How is graft rejection treated?

A

By immunosuppresive drugs (that inhibit immune responses against the graft)

60
Q

Transplantation of hematopoietic stem cells (HSCs) requires careful matching of donor and recipient. What (common) complications can occur?

A

graft-vs-host disease (GVHD) and immune deficiency

61
Q

What is the cause of primary (inherited) immune deficiency diseases?

A

These diseases are caused by inherited mutations in genes involved in lymphocyte maturation or function, or in innate immunity.

62
Q

What are some common disorders affecting lymphocytes and the adaptive immune resonses?

(idk to what extend you have to learn these)

A

• X-SCID: Failure of T cell and B cell maturation; mutation in
the common γ chain of a cytokine receptor, leading to failure
of IL-7 signaling and defective lymphopoiesis
• Autosomal recessive SCID: Failure of T cell development; secondary defect in antibody responses; approximately 50% of cases caused by mutation in the gene encoding ADA, leading to accumulation of toxic metabolites during lymphocyte
maturation and proliferation
• X-linked agammaglobulinemia (XLA): Failure of B-cell maturation, absence of antibodies; caused by mutations in the BTK gene, which encodes B-cell tyrosine kinase, required for maturation signals from the pre–B-cell and B-cell receptors
• Di George syndrome: Failure of development of thymus, with T cell deficiency
• X-linked hyper-IgM syndrome: Failure to produce isotypeswitched high-affinity antibodies (IgG, IgA, IgE); mutations in genes encoding CD40L or activation-induced cytosine deaminase
• Common variable immunodeficiency: Defects in antibody production; cause unknown in most cases.
• Selective IgA deficiency: Failure of IgA production; cause unknown

63
Q

What do the deficiencies in the innate immunity include?

A

Defects of leukocyte function, complement and innate immune receptors

64
Q

What do primary (inherited) immune deficiency diseases clinically present with?

A

Increased susceptibility to infections in early life

65
Q

What does HIV stand for?

A

Human immunodeficiency virus

66
Q

What are the steps of the HIV life cycle?

A
  • virus entry into cells
  • viral replication
  • progression of infection/virus release
67
Q

How are HIVs entered into cells?

A

It requires CD4 and coreceptors, which are receptors for chemokines; involves binding of viral gp120 and fusion with the cell mediated by viral gp41 protein; main cellular targets: CD4+ helper T cells, macrophages, DCs

68
Q

How does viral replication of HIVs occur?

A

Integration of provirus genome into host cell DNA; triggering of viral gene expression by stimuli that activate infected cells (e.g., infectious microbes, cytokines produced during normal immune responses)

69
Q

How does an infection of HIVs progress?

A

Acute infection of mucosal T cells and DCs; viremia with dissemination of virus; latent infection of cells in lymphoid tissue; continuing viral replication and progressive loss of CD4+ T cells

70
Q

What are the mechasnisms of immune deficiency (in regard to HIVs)?

A

• Loss of CD4+ T cells: T cell death during viral replication and
budding (similar to other cytopathic infections); apoptosis occurring as a result of chronic stimulation; decreased thymic output; functional defects
• Defective macrophage and DC functions
• Destruction of architecture of lymphoid tissues (late)

71
Q

Explain (clinically) the progression/phages of HIV disease

A

• Acute HIV infection. Manifestations of acute viral illness
• Chronic (latent) phase. Dissemination of virus, host immune
response, progressive destruction of immune cells.
• AIDS. Severe immune deficiency.

72
Q

What are the clinical complications of HIV?

A

Full-blown AIDS manifests with several complications, mostly resulting from immune deficiency.
• Opportunistic infections
• Tumors, especially tumors caused by oncogenic viruses
• Neurologic complications of unknown pathogenesis

73
Q

How is HIV treated?

A

With antiretroviral therapy

74
Q

What is amyloidosis?

A

Amyloidosis is a disorder characterized by the extracellular deposits of proteins that are prone to aggregate and form insoluble fibrils.

75
Q

What may the deposition of proteins (that are prone to aggregate and form insoluble fibrils) result from (in amyloidosis)?

A

excessive production of proteins that are prone to aggregation; mutations that produce proteins that cannot fold properly and tend to aggregate; defective or incomplete proteolytic degradation of extracellular proteins.

76
Q

Is amyloidosis localized or systemic?

A

Can be either!

77
Q

Amyloidosis is seen in association with a variety of primary disorders. Name some.

A
  • Monoclonal B-cell proliferations (in which the amyloid deposits consist of immunoglobulin light chains);
  • chronic inflammatory diseases such as rheumatoid arthritis (deposits of amyloid A protein, derived from an acute-phase protein produced in inflammation);
  • Alzheimer disease (amyloid β protein); familial conditions in which the amyloid deposits consist of mutated proteins
  • hemodialysis (deposits of β2-microglobulin, whose clearance is defective).
78
Q

Amyloid deposits cause tissue injury and impair normal function by …

A

causing pressure on cells and tissues.

79
Q

Do amyloid deposists evoke an inflammatory respons?

A

Nope

Pathology (28 decks)

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