Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

B&L Unit 1 and 2 > Immunology > Flashcards

Immunology Flashcards

1
Q

Type I immunopathology (basic definition)

A

immediate hypersensitivity, is seen in patients who make too much

IgE to an environmental antigen, which is often innocuous like a pollen or food.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type II immunopathology (basic definition)

A

autoimmunity due to antibodies which react against self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type III immunopathology (basic definition)

A

immune complexes of antigen and antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type IV immunopathology (basic definition)

A

T cell mediated, and can be autoimmune, or more commonly innocent bystander injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Severe Combined Immunodeficiency Disease (SCID)

What enzyme is absent?

A
  • block in development of the lymphoid stem cell, or its further maturation
  • lymphopenia of both T and B cells
  • worst of the immunodeficiency states

~adenosine deaminase (ADA) deficiency > accumulation of adenosine
~ transplantation: fetal thymus graft, bone marrow transplantation, purified stem cells
~ Gene replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

X-linked (Bruton) agammaglobulinemia

A
  • developmental block b/t pre-B cell and B cell
  • a protein tyrosine kinase gene, btk, normally expressed in preB and later B cells, is defective
  • normal T cells but low to absent B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

X-linked HyperIgM syndrome

A
  • defect in the IgM-to-IgG switch mechanism
  • The Tfh cell has an accessory molecule (CD40-ligand) that interacts with CD40 on B cells, signaling them to switch classes
  • If either molecule is defective, the B cell is driven hard but can’t be instructed to switch past making IgM
  • high IgM with low IgG and IgA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Common Variable Immunodeficiency (CVID)

A
  • normal numbers of pre-B cells and B cells, but the B cells are difficult to trigger to make specific antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DiGeorge Syndrome

A
  • large (45 gene) deletion on chromosome 22
  • stroma of thyroid will not support thymic lymphoid development
  • absent T cells with normal B cells

~ unexplained convulsions controllable by calcium
~ great vessels of the heart develop abnormally
~ hypertelorism (increased distance between eyes), down-slanting eyes, fishmouth deformity, micrognathia (jaw undersized), and low-set ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

blank

A

blank

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Incidence of selective IgA deficiency

A

~ most common immunodeficiency disease: 1 in 500

~ syndromes: diarrhea and sinopulmonary infections, or an increased frequency and severity of allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nude mouse

A

~fail to make a thymic stroma (and hair) and so they have no T cells, and are immunologically similar to DiGeorge kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2 Mechanisms for Type 2 Autoimmunity

A
  1. Complement-mediated damage. Tissues against which antibodies are made can be damaged by lysis, by phagocytosis, or by release of the phagocytes’ lysosomal enzymes and reactive oxygen species (probable in myasthenia gravis and Goodpasture disease).
  2. “Stimulatory hypersensitivity.” If the autoantibody happens to be directed against a cell surface receptor, it may behave as an agonist, mimicking whatever hormone or factor normally works at that receptor.

> antibody binds to receptor, mimics the actual ligand and activates that receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Myasthenia Gravis

A
  • Type II
  • disease of progressive muscle weakness
  • make antibodies to acetylcholine receptor
  • damage is complement and neutrophil-mediated
  • thymic transcription factor (Aire) drives thymic expression of receptor
  • without it, there is no negative selection against Th cells that are reactive with that receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rheumatic Heart Disease

A
  • Type II
  • heart disease occurring shortly after a streptococcal infection
  • cross-reaction between a Group A Streptococcus M-protein antigen and a structure on the heart’s endothelial lining, probably laminin on heart valves, followed by neutrophil-mediated tissue destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dressler Syndrome

A
  • Type II

- Most people who have a heart attack will make some autoantibody which reacts with heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Goodpasture Syndrome

A
  • Type II
  • formation of autoantibodies to lung and kidney basement membranes (where the endothelial cells of capillaries sit)
  • antigen shared b/t these two organs
  • persistent glomerulonephritis and pneumonitis w/ pulmonary hemorrhages
  • In Goodpasture the antibody is directed against the basement membrane, not trapped as clumps, so the staining by immunofluorescence is sharp and ‘linear,’ not ‘lumpy-bumpy’ as it is in Type III, immune complex conditions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Autoimmune Thrombocytopenic Purpura

A
  • Type II
  • bleeding abnormalities due to destruction of platelets
  • platelets are opsonized and destruction (mostly in spleen) is rapid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Autoimmune Hemolytic Anemia

A
  • Type II
  • antibody against RBCs causing them to lyse
  • can be temporarily drug-induced, assoc. w/ other autoimmune syndrome, cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Systemic Lupus Erythematosus

A
  • Type II
  • may make antibody to: nuclear and nucleolar proteins; DNA; RNA; erythrocytes; clotting factors; platelets; skin; and T cells
  • both autoantibodies and autoreactive T cells are implicated in the pathogenesis, so they are mixed Type II and Type IV mechanisms
21
Q

Rheumatoid Arthritis

A
  • Type II
  • inflammatory arthritis
  • most common autoimmune disease
  • rheumatoid factor: IgM anti-IgG (antibody against antibody)
22
Q

Hashimoto Thyroiditis

A
  • Type II
  • inflammatory disease of thyroid, most likely T and B cell immunity to thyroid antigens
  • antibodies to thyroid antigens are destructive, not stimulatory
23
Q

Goodpasture Immunofluorescence Test

A
  • In Goodpasture the antibody is directed against the basement membrane, not trapped as clumps, so the staining by immunofluorescence is sharp and ‘linear,’ not ‘lumpy-bumpy’ as it is in Type III, immune complex conditions.
24
Q

Innocent bystander phenomenon

A

a common mechanism, in which there is damage to normal tissue which happens to be associated with or infected by the antigen, which is truly foreign

25
Q

Describe how antibody-mediated tissue damage could result from coupling self antigen with a foreign antigenic “carrier”

A

1) B cell binds self plus foreign epitope
2) Ingests and digests
3) Presents foreign epitope to Th2 on Class II MHC
4) Tfh releases cytokines, engages coreceptors
5) B cell is activated, secretes antibody to self

26
Q

Rheumatoid Factor

A
  • antibody against the Fc portion of IgG
  • although predominantly encountered as IgM, Rheumatoid factor can be of any isotype of immunoglobulins, IgA, IgG, IgM IgE IgD
27
Q

Name a condition in which antibody stimulates rather than inhibits or harms its target cell

A

Graves disease
Stimulatory hypersensitivity: LATS, as it was called for a long time, is simply an IgG antibody to the TSH (thyroid-stimulating hormone) receptor on thyroid cells; when it binds to these receptors, it mimics TSH and causes the cell to secrete thyroid hormones. Of course, the normal feedback controls won’t work in this case, so the result is hyperthyroidism

28
Q

Graves disease

A
  • Type II
  • Stimulatory hypersensitivity: LATS, as it was called for a long time, is simply an IgG antibody to the TSH (thyroid-stimulating hormone) receptor on thyroid cells; when it binds to these receptors, it mimics TSH and causes the cell to secrete thyroid hormones. Of course, the normal feedback controls won’t work in this case, so the result is hyperthyroidism
29
Q

Discuss how the Aire gene is involved in preventing autoimmune disease.

A

AIRE is a transcription factor expressed in the medulla of the thymus and controls the mechanism that prevents the immune system from attacking the body itself. AIRE causes transcription of a wide selection of organ-specific genes that create proteins that are usually only expressed in peripheral tissues, creating an “immunological self-shadow” in the thymus. It is important that self-reactive T cells that bind strongly to self-antigen are eliminated in the thymus (via the process of negative selection), otherwise they can later bind to their corresponding self-proteins and create an autoimmune reaction. When AIRE is defective, T cells can attack the body, resulting in autoimmune disease.

30
Q

Define Type IV immunopathology.

A

T cell-mediated immunity and delayed hypersensitivity

- only type of immunopathology (of Types I, II, III and IV) which do not require antibody or B cells

31
Q

Differentiate between a first-set and second-set graft rejection.

A
  • Type IV

First set reaction: 10-20 days

  • 5% T cells recognize foreign MHC as MHC + peptide
  • response to that foreign graft antigen is boosted, develops more anti Th1 and CTL

Second set reaction: 5-10 days
- faster response due to memory T cell development during first exposure

32
Q

Discuss the three requirements for graft-versus-host disease to occur.

A
  1. The graft must contain immunocompetent T cells (even bone marrow has mature T cells in it).
  2. There must be at least one antigen in the host which the graft’s T cells can recognize (so, no worries with identical twins.)
  3. The host must be relatively immunoincompetent or unable for genetic reasons to recognize the graft’s MHC antigens, otherwise the graft would be rejected too rapidly.
33
Q

Speculate on the role of HLA alleles in autoimmunity and chronic inflammatory diseases.

A

The human leukocyte antigen (HLA) system is the locus of genes that encode for proteins on the surface of cells that are responsible for regulation of the immune system in humans. The HLA genes are the human versions of the major histocompatibility complex (MHC) genes that are found in most vertebrates (and thus are the most studied of the MHC genes).

Damaged HLA (aka MHC) might bind self-peptides that are not normally presented > autoimmunity

34
Q

. Describe the factors that regulate the differentiation of Th0 cells in the Peyer’s Patches to Th1, Th2, or Th17 versus into Treg cells.

A

Cytokine TGFβ in the submucosal Peyer’s Patches that favors the differentiation of Th0 cells into Treg. Dendritic cells here make IL-10 and that also favors Treg development.

►However, the combination of TGFβ and IL-6 has been shown to downregulate Treg and
upregulate Th1, Th2, and Th17. IL-6 is produced by epithelial and other cells in response to stress or damage.

Treg tells Th not to react to normal gut flora. When the innate response indicates a threat, it makes stress cytokines like IL-6 and the response switches from Treg production to defensive Th1, Th17, or Th2.

35
Q

Celiac disease

A
  • chronic frustrated immune response
  • antigen is tissue transglutaminase 2 (TG2)
  • makes protein crosslinks through glutamines
  • if it couples to but can’t release digestion-resistant, glutamine-rich gliadin (wheat) peptides, inadvertently turn itself into a B-cell autoantigen by the ‘foreign + self hybrid antigen’ help mechanism
  • it is T cell immunity to gliadin peptides that is responsible for the chronic inflammation
  • 90% have HLA-DQ2
36
Q

Chronic beryllium disease

A
  • chronic frustrated immune response

- Inhaled Be > creates novel epitopes to which a Th1 response is made, and later a scarring Th2 response as well

37
Q

Mechanism of Type I

A

A person with a worm infestation will make both IgE and IgG against them. The IgG binds the worm or its ova, activates complement (to the lytic effects of which worms are impervious) and C3a and C5a attract neutrophils. They arrive, seize the opsonized worm with their IgG and C3 receptors, and…nothing. Neutrophils lack a helminthocidal mechanism.

That’s where IgE comes in. As the worm sheds antigens they diffuse to nearby mast cells, whose FcεR have become loaded with anti-helminth IgE. Antigen cross-links the IgE and the mast cells degranulate. Histamine causes gut smooth muscle contraction, and violent peristalsis can help expel worms. But the real action is in the late-phase response, where prostaglandins and leukotrienes are elaborated by the mast cell; as “ECFA” they attract eosinophils in large numbers. Like other phagocytes, eosinophils have Fc receptors for IgG, which as we’ve noted is coating the worm. When an eosinophil engages an opsonized worm it release the contents of its granules, which include Major Basic Protein (the reason eosinophils bind the acidic dye eosin). ►MBP is highly toxic to helminths.

38
Q

Describe the mechanism of IgE-mediated hypersensitivity in terms of: IgE attachment to basophils or mast cells; reaction with allergens; mediator release; effects of mediators on target tissues and cells.

A

IgE binds strongly to FcεR1 receptors on the surface of mast cells (and basophils). When 2 adjacent IgE molecules so bound are cross-linked by allergen, the mast cell is signaled to release the contents of its characteristic granules, including histamine, which causes local or systemic vasodilation and increased permeability, and gut and bronchial smooth muscle contraction.

39
Q

Describe the immediate allergic reaction and the late-phase reaction in terms of the time course of the reaction and mediators involved.

A

Two phases. The immediate reaction is due to histamine, and can be blocked effectively by antihistamines, which are receptor antagonists. The late phase, beginning perhaps 4 to 10 hours later, is not affected by antihistamines, as it depends on prostaglandins, leukotrienes, and cytokines. Needs anti-inflammatory meds.

.- Eosinophils also attracted to IL-4 released by Th2. Cytokines are also released by the mast cell.

40
Q

Mechanism of Type III

A
  • too large to pass readily through the basement membranes of small blood vessels and so get stuck in the basement membrane.
  • there, they activate complement by binding C1q and initiating the classical complement cascade
  • C3a and C5a attract neutrophils and release histamine and other mediators from mast cells, increasing the inflammatory reaction.
41
Q

One-shot Serum Sickness

A
  • Type III
42
Q

Arthus Reaction

A
  • Type III
  • booster immunization
  • patient has pre-existing antibody to the immunogen (it may be cross-reactive) so that when the antigen is deposited by injection, complexes immediately begin to form locally
43
Q

Farmer’s Lung

A
  • Type III

- filamentous bacteria

44
Q

Post-streptococcal Glomerulonephritis

A
  • Type III

- antigen: strep

45
Q

Rheumatoid Arthritis:

A
  • Type III

- rheumatoid factor is IgM antibody to own IgG

46
Q

Systematic Lupus Erythematous

A
  • Type III

- IgG antibody to double stranded DNA- immune complexes deposit preferentially in the kidney > glomerulonephritiss

47
Q

IgA Neuropathy

A
  • Type III
  • most common form of glomerulonephropathy in the world
  • co-deposition of IgA and IgG in the renal glomerulus
  • antibodies IgA or IgG bind underglycosylated IgA1 and complexes form
48
Q

Cryoglobin

A
  • related to Type III
  • Test for immune complexes
  • cryoglobins are fluffy white precipitate
  • mixed cryoglobins, being antigen + antibody;
  • single component cryoglobins are monoclonal product of malignant B cells
49
Q

Fluorescence of Type III

A
  • lumpy bumpy

- tiny clumps of antigen-antibody complex

B&L Unit 1 and 2 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions