Immune Flashcards

1
Q

REQUIREMENTS OF AUTOIMMUNITY

A

● The presence of an immune reaction specific for some self antigen or self tissue
● Not secondary to tissue damage but is of primary pathogenic significance
● Absence of another well-defined cause of the disease

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

Diseases mediated by antibodies

A
Hemolytic anemia
Thrombocytopenia
atrophic gastritis of pernicious anemia
Myasthenia gravis
Graves disease
goodpasture syndrome
SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diseases mediated by T cells

A
T1 DM
Multiple sclerosis
Rheumatoid arthritis
Systemic sclerosis
Sjogen sydndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diseases postulated to be autoimmune

A
IBD
Primary biliary cirrhosis
Autoimmune hepatits
Polyarteritis nodosa
Inflammatory myopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phenomenon of unresponsiveness to an antigen
induced by exposure of lymphocytes to that
antigen

A

IMMUNOLOGIC TOLERANCE

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

CENTRAL TOLERANCE:

Originates in the_______

A

primary lymphoid organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Process where your immature T cells
express receptors specific to self
antigen. When these proliferate, they are
self reactive. The body kills these cells
through apoptosis

A

Negative Selection or clonal deletion

T cells (thymus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stimulates expression of
some peripheral tissue restricted self
antigens in the thymus and is thus critical
for deletion of immature T cells specific
for these antigens

A

AIRE (autoimmune

regulator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cells are still intact but the receptor is
changed into another type so that the
potentially reactive lymphocyte will no
longer react to its own tissue.

A

● Receptor Editing

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

This occurs when self-reactive cells escape the
central lymphoid organs reaching the periphery
and so the mechanisms are also different.

A

PERIPHERAL TOLERANCE

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

The best-defined regulatory T
cells are___ cells that express high
levels of CD25, the α chain of the IL-2
receptor, and FOXP3,

A

CD4

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

Activation of antigen-specific T cells

requires two signals:

A
recognition of 
peptide antigen in association with self 
MHC molecules on the surface of APCs 
and a set of costimulatory signals 
(“second signals”) from APCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

binds ligand of T cell from your APC.
If this signal is absent or is unresponsive
there is no binding. This is failure to
respond

A

co-stimulatory signal (such as CD28),

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

HLA associated diseases

A
RA
T1 DM
Multiple sclerosis
SLE
Ankylosing spondylitis (100-200)
Celiac disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which
encode your tyrosine phosphatase and involved
in Rheumatoid Arthritis and Type 1 DM and
Inflammatory bowel disease

A

genes associated with your PTPN22

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Best known for inflammatory bowel
disease.
- associated with crohn’s disease

A

NOD2

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

Polymorphisms in the gene encoding
the IL-2 receptor (CD25) are associated
with

A

Multiple sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

antibodies against strep proteins
cross react with myocardial proteins and cause
myocarditis. The immune responses initially
directed against microbial antigens, also result in
activation of self-reactive lymphocytes. Aside
from attacking just the strep protein, it also
attacks own tissue

A

Rheumatic Heart Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Some viruses, such as EBV and HIV, cause _______, which may result
in production of autoantibodies.

A

polyclonal B-cell activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T or F
infections promote low-level
IL-2 production, and this is essential for
maintaining regulatory T cells

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In addition to infections, _____causes cell death and may lead to the
exposure of nuclear antigens, which elicit
pathologic immune responses in lupus; this
mechanism is the proposed explanation for the
association of lupus flares with exposure to
sunlight.

A

ultraviolet (UV)

radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T or F
Smoking is a risk factor for rheumatoid arthritis,
perhaps because it leads to chemical
modification of self antigens.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Autoimmune disease involving multiple organs,
characterized by a vast array of autoantibodies,
particularly antinuclear antibodies (ANAs), in
which injury is caused mainly by deposition of
immune complexes and binding of antibodies to
various cells and tissues

A

SYSTEMIC LUPUS ERYTHEMATOSUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In SLE, injury to the _____________ is prominent.

The disease is very heterogeneous, and any
patient may present with any number of these
clinical features

A

skin, joints, kidney, and serosal

membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

SLE is a Type___Hypersensitivity Reaction

A

III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Clinical/immunologic criteria: (this is important to

the diagnosis of SLE) cutaneous lupus ____(acute) & ____ (chronic).

A

malar rash; discoid rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

A RASH POINT MD

A

Mnemonic: A RASH POINT MD
● Arthritis
● Renal disease, ANAs, Serositis, Hematological
disorders
● Photosensitivity, Oral Ulcers, Immunological
Disorders, Neurological Disorders
● Malar Rash, Discoid ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

For a patient to be classified having SLE you need to have ______ both have clinical and
immunological.

A

4/11 of criterion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

The hallmark of SLE is the production of

autoantibodies, several of which (_________) are virtually diagnostic

A

antibodies to
double-stranded DNA and the so called Smith
[Sm] antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ANA’s. These are directed against nuclear Ag
and can be grouped into four categories based
on their specificity for:

A

○ DNA
○ Histones
○ Non histone proteins bound to RNA
○ Nucleolar Ag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

is the most
widely used method for detecting ANA, which can
identify Ab that binds to a variety of nuclear Ag.
The pattern of nuclear fluorescence suggests the
type of Ab present in a patient’s serum

A

Indirect Immunofluorescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

● Antibodies to chromatin, histones and
occasionally, double stranded DNA
● Most specific

A

Homogenous or diffuse nuclear staining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Most often indicative antibodies to double

stranded DNA and nuclear envelope proteins

A

Rim or peripheral staining

34
Q

● Presence of uniform or variable-sized speckles
● Most commonly observed patterns of
fluorescence and therefore the least specific
● Antibodies to non-DNA nuclear constituent such
as Sm antigen(SLE), ribonucleoprotein (SLE and
others) and SS-A and SS-B (Sjogren)

A

Speckled pattern (

35
Q

● Antibodies specific for centromeres (Systemic
sclerosis, Sjogren)
● Stain Ab to centromere

A

Centromeric pattern

36
Q

● Ab to RNA
● Presence of few discrete spots of fluorescence
within the nucleus.
● Most often in patients with systemic sclerosis

A

Nucleolar pattern

37
Q

SLE- most specific is _______ and also
associated with _____.
Generic ANA involved there are 95 to 100
percent positive for SLE, but the problem for this
is not specific. Sm antigen there is 20-30 percent
positive

A

Sm antigen; Antiphospholipid syndrome

38
Q

is specific for CCP (cyclic

citrullinated peptides)

A

Rheumatoid arthritis

39
Q

The fundamental defect in SLE is a failure of the

mechanism that maintains___________

A

self-tolerance

40
Q

T OR F
Lack of your complement may impair removal
of circulating immune complexes by
mononuclear phagocyte system and since they
are not removed, favoring deposition in the
tissues, leading to tissue anergy

A

T

41
Q

T or F
There is a higher rate of concordance (>20%) in
monozygotic twins when compared with
dizygotic twins (1% to 3%).

A

T

42
Q

Specific alleles of the _______ locus have been
linked to the production of anti–double-stranded
DNA, anti-Sm, and antiphospholipid antibodies,
although the relative risk is small

A

HLA-DQ

43
Q

play a role in lymphocyte

activation in SLE.

A

Type I interferons

-are antiviral
cytokines that are normally produced during
innate immune responses to viruses.

44
Q

T or F
The autoantibodies in
SLE show characteristics of T cell-dependent
antibodies produced in germinal centers, and increased numbers of follicular helper T cells
have been detected in the blood of SLE patients.

A

T

45
Q

TLR engagement by nuclear DNA and RNA

contained in immune complexes may activate______

A

B lymphocytes

46
Q

Drugs such as ___________can induce an SLE- like

response in humans

A

hydralazine, procainamide, and

D-penicillamine

47
Q

● Most common mechanism of tissue injury
● DNA and anti-DNA complexes deposit in the glomeruli and small blood vessels, and they go into tissues resulting in a low level of serum
complement. Because they are deposited in
glomeruli and other tissues

A

Deposition of Immune complexes (Type 3

Hypersensitivity

48
Q
Most common disorder caused is Immune 
Thrombocytopenic Purpura (ITP)
A

Autoantibodies specific for RBCs, WBCs and

platelets (Ab-mediated type 2 hypersensitivity)

49
Q

● Secondary APS
● Venous and arterial thrombosis associated with
recurrent spontaneous miscarraige and focal
cerebral or ocular ischemia

A

Antiphospholipid antibody Syndrome (APS)

50
Q

Antibodies cross the BBB and react with
receptor or neuron for various neurotransmitter
● Cytokine may involved in cognitive dysfunction

A

Neuropsychiatric manifestations

51
Q

Nuclei of damaged cells
react with your ANAs, they lose their chromatin
and become a homogenous material to produce_______

A

LE body

52
Q

Usually seen in blood vessels and usually
manifested as thrombosis (venous or arterial) or
vasculitis. Mechanism for patients with recurrent
miscarriages because of antiphospholipid
antibodies.

A

Antinuclear Antibodies

53
Q

In SLE, the most clinical involvement is the ____

A

Kidney (50% of SLE patients)

54
Q

Class 1 glomerular patterns

-is very uncommon and is characterized by immune complex deposition in the mesangium

A

Minimal mesangial lupus nephritis

-No infiltrates yet but Mesangial deposits are present by IgG (granular type)

55
Q

Class 2 glomerular patterns

A

MESANGIAL PROLIFERATIVE LUPUS

NEPHRITIS

56
Q

Class 1 are identified by ______

A

IF and EM

57
Q

● Mesangial proliferation often with accumulation
of mesangial matrix and granular mesangial
deposits of immunoglobulins and complement
● No involvement of capillaries

A

Class 2 Mesangial proliferative lupus nephritis

58
Q

Class 3 glomerular patterns

A

Focal lupus nephritis

59
Q

● <50% glomeruli involved (segmental-portion or
global-affects whole)
● Endothelial and mesangial cell proliferation
● Leukocyte accumulation
● Capillary necrosis and hyaline thrombi
● Extracapillary proliferation
● Crescent formation
● With hyaline thrombi (pink material) meaning
there is involvement of capillaries

A

Class 3: Focal lupus nephritis

60
Q

The clinical presentation ranges from mild hematuria and proteinuria to acute renal insufficiency.

A

Class 3: Focal lupus nephritis

61
Q

Class 4 glomerular patterns

A

Diffuse lupus nephritis

62
Q

● Most common type
● Severe form
● >50% glomerular involvement

A

CLASS 4 : DIFFUSE LUPUS NEPHRITIS

63
Q

● Endothelial, mesangial and epithelial cell
proliferation
● Crescent formation
● “Wire loop” lesion - subendothelial deposits

A

CLASS 4 : DIFFUSE LUPUS NEPHRITIS

64
Q

Class 5 glomerular patterns

A

MEMBRANOUS LUPUS NEPHRITIS

65
Q

● Same with class 4
● PAS stain, capillaries are well distinct because of
thickening
● This patient has severe proteinuria
● Diffuse thickening of capillary walls due to
subepithelial deposits

A

CLASS 5: MEMBRANOUS LUPUS NEPHRITIS

66
Q

The immune complexes are usually accompanied by increased production of basement membrane-like material.

A

Class 5: membranous lupus nephritis

67
Q

Class 6 glomerular patterns

A

ADVANCED SCLEROSING NEPHRITIS

68
Q
● >90% glomerular involvement
● End-stage renal disease 
● With lots of fibrosis and fibrinoid necrosis of 
tubules and arterioles, 
● Kidneys are not functional anymore
A

CLASS 6: ADVANCED SCLEROSING NEPHRITIS

69
Q

TUBULOINTERSTITIAL LESION

A

● Immune complexes in tubular or peritubular
capillaries
● Well-organized B cell follicles in the interstitium

70
Q

Thick capillary loop no longer delicate so this
produces characteristic wire loop lesions so as
you can see here is quietly thick already

A

SLE

71
Q

In SLE, there is vacuolar degeneration of basal layer in this area

A

Epidermis

72
Q

In SLE, variable edema and perivascular

inflammation occur in this area

A

Dermis

73
Q

endocarditis associated with the

use of steroids

A

Libman sacks endocarditis

74
Q

T or F
Vegetation in infective endocarditis are
smaller and confined to the lines of closure of the
valve leaflets

A

False

Vegetation in Rheumatic heart disease are
smaller and confined to the lines of closure of the
valve leaflets

75
Q

In SLE, Central penicilliary arteries show concentric
intimal and smooth muscle cell hyperplasia
producing _________

A

Onion-skin lesions

76
Q

● Skin manifestations of SLE but rare systemic
manifestations
● Skin plaques with varying degrees of edema,
erythema, scaliness, follicular plugging and skin
atrophy surrounded by an erythematous border
● (+) generic ANAs, (-) anti-dsDNA

A

CHRONIC DISCOID LUPUS ERYTHEMATOSUS

77
Q

CHRONIC DISCOID LUPUS ERYTHEMATOSUS:

IF: _____ deposition at dermoepidermal
junction

A

Ig and C3

78
Q

● Intermediate between SLE and chronic discoid
lupus
● Predominant skin involvement
● Skin rash is widespread, superficial and nonscarring
● Mild systemic symptoms consistent with SLE
● (+) anti-SSA and HLA-DR3 phenotype

A

SUBACUTE CUTANEOUS LUPUS

ERYTHEMATOSUS

79
Q

● Induced by: Hydralazine, procainamide, isoniazid
and D-penicillamine
● Anti-TNF therapy
+ anti-histone antibodies

A

DRUG-INDUCED LUPUS ERYTHEMATOSUS

80
Q

● chronic inflammatory disease that involves the
joints with subsequent involvement of the extra
articular tissues such as the skin, blood vessels,
lungs, and heart

A

RHEUMATOID ARTHRITIS

81
Q

● Chronic disease characterized by:

1) dry eyes (keratoconjunctivitis sicca
(2) dry mouth (xerostomia)

A

SJOGREN SYNDROME

82
Q

aka Sicca syndrome

A

Primary sjogen syndrome