Immune System Flashcards

1
Q

Natural Killer cells

A

Carry marker CD 16
Kill cells with downregulated MHC class 1 and stress related Fc fragments-virus infected cells and tumour related cells
Release perforins which lyse cells

Respond to IFN and IL-2

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

MHC Class 1, 2 and 3 locations

A

MHC 1: All nucleated and platelet cells
Coded by HLA A, B and C

MHC 2: Macrophages, activated T cells, B cells and dendritic cells

MHC 3: Complement

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

Antigen presentation

A

MHC Class 1: Endogenous protein such as viral protein is presented by MHC class 1 and detected by CD 8+ T Cells

MHC Class 2: Exogenous protein such as phagocytosed material is presented by MHC class 2 and detected by CD 4+ T helper Cells

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

T cells, TCR and MHC

A

T cells recognise MHC via their own TCR

CD 4 T helper cells recognise MHC 2 and CD8 T cells recognise MHC 1

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

CD8 T cells

A

MHC Class 1 –> CD 8 T cells

Kill cells and leave memory cells behind

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

CD4 T Helper Cells

A

Recognise MHC Class 2:
IFN g—>macrophages
IL-2—>T cell and B cell proliferation
IL-4—>promotes CD4 T cells and B cell proliferation
IL-5—>activation of eosinophils
IL-6—>T cell and B cell differentiation
IL-10—>Suppresses macrophage cytokine production
IL-12—>Promotes cytotoxic action of T and B cells

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

B cells

A

B cells detect antigen via B cell receptor and then morph into plasma cells which secrete immunoglobulins

CD4 T helper cells (activated by MHC class II) promote Ig production

All Ig have similar structure except IgM

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

Hypersensitivity reactions Type I-V

A

Type 1: Immediate/Anaphylaxic Ig E
Asthma, anaphylaxis

Type 2: Ig to ag Cytotoxic
Drug reaction, autoimmune thrombocytopenia, transfusion reaction

Type 3: Ig/Ag Immune complexes
SLE, glomerulonephritis

Type 4: CD 8 T Cells
TB mantoux, transplant rejection

Type 5: Anti-receptor ab’s
Grave’s myasthenia gravis

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

Autoantibodies

A
ANA ---> SLE, Sjogrens
Anti-Ro ---> Sjogrens
Anti-La ---> Sjogrens
Anti-centromere ---> CREST
Anti-Scl70 ---> Scleroderma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MHC Class 1 and 2 diseases

A

MHC 1: More in men

  • HLA b27 (Ankylosing spondylitis and Reiter’s syndrome)
  • HLA Cw6 (Psoriasis)

MHC Class II: More in women

  • HLA-DR5 (Pernicious anaemia and Hashimoto’s)
  • Rheumatoid Arthritis (HLA-DR4)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Immune deficiency (6)

A
IgA Deficiency
Common variable immunodeficiency
Brutons' x-linked agammaglobulinaemia
Subacute combined immunodeficency
Di-George's syndrome
Complement factor deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

IgA Deficiency

A

Congenital or acquired (post virus)

Recurrent pulmonary/Gi infections

Usually asymptomatic

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

Common variable immunodeficiency

A

Congenital

Hypogammaglobulinaemia particularly IgG

Recurrent pyogenic infections after first decade

Autoimmune disease and lymphoid malignancy

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

Brutons’ x-linked agammaglobulinaemia

A

X-linked

No B cells therefore no Ig

T cells function normal

Recurrent bacterial infections, viral and fungal infection normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Di-Goerge Syndrome

A

Congenital-damage to 3rd and 4th pharyngeal pouches due to 22q11 (CATCH 22)

  • CARDIAC (Aortic arch-heart failure)
  • ATRESIA (Oesophageal)
  • THYMIC (Hypoplasia)
  • CLEFT palate (Dysmorphic facies)
  • HYPOCALCAEMIA (parathyroid hypoplasia)

T cell deficiency=Viral and parasitic disease
B cells normal

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

Severe Combined immunodeficiency

A

Autosomal or x-linked recessive disease
T cell, B cell and lymphopenia
Death <1 year unless bone marrow transplant

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

Complement factor deficiency

A

C2-Autoimmune connective tissue disorder
C3-bacterial infections
C5-8 Recurrent Neisseria infections

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

Infections usually killed by spleen

A

Encapsulated organisms:

Strep. pneumoniae
Neisseria Meningitidis
Haemophilus influenzae

19
Q

Post splenectomy vaccination

A

HiB vaccine and meningococcus vaccine prior to or after surgery

Pen V or erythromycin life long

20
Q

Complement and B cell deficiency causes

A

pyogenic bacteria:
Staphy
Strep
Haemophilus

Neisseria

21
Q

Phagocyte deficiency

A

Staph
Gram negative
Fungal

22
Q

T cells

A

Opportunistic infections

23
Q

Kostmann’s syndrome

A

Congential neutrophilia

24
Q

Leukocyte adhesion deficiency

A

No ability for chemotaxis

25
Q

Chronic granulomatous disease

A

X linked

NADPH oxidase deficiency

26
Q

Classical pathway

A

Antigen and antibody complex

activates C1 into C1s

C1s signals C4 and C2 into C4b and C2b

these combine into C4bC2b (C3 convertase)

27
Q

MBL pathway

A

MBL is lectin like molecule

MBL binds to mannose on foreign cell

activates MASP-2—>C4/C2 into C3 convertase

28
Q

Alternative pathway

A

Stimulated by bacterial cell wall components e.g. teichoic acid, LPS

spontaneously form C3b

29
Q

C3 converatse

A

C3 becomes:

C3a-Anaphylatoxin
C3b-Opsonin (Cr1 from neut binds to C3b-phagocytosis)
C3b-Forms C5 convertase

30
Q

C5 Converstase

A

C5a-anaphylatoxin and chemokine for neut.

C5b-actuvates C6, 7, 8 and 9 to form MAC

31
Q

Complement deficiencies

A

Classical pathway deficiency

  • SLE
  • Immune complexes not cleared

MBL pathway deficiency

  • Common
  • Only problematic in immunosuppression

Alternative pathway
-Encapsulated bacteria

32
Q

C3 deficiency

A

Bacterial infections

Membranoproliferative glomerulonephritis

33
Q

Terminal common pathway

A

C5-9
Encapsulated bacteria
(Neisseria Meningitis, N. gonorrhoa, strep pneumonia, haemophilus)
Meningitis

34
Q

T cell defects affect B cells

A
Because CD 4 helper cells cause B cell class switching
So IgM is normal but low IgG and IgA
35
Q

ANA detects

A

SLE, Sjogrens, Scleroderma
Polymyositis,Dermatomyositis
Sensitive=No ANA no SLE
not specific=Positive-can be other things

36
Q

Autoabs

A

dsDNA-normal SLE
Histones-drug induced SLE

Speckled RNP-SLE, MCTD
Speckled Smith-SLE
Speckled Ro/LA- SLE and Sjogrens
Speckled Jo-1POly/dermatomyositis

Centromere LC Scleroderma

Nucleolar scl-70 DC scleroderma
Nucleolar RNA-pol DC Scleroderma

37
Q

ANCA

A

C-ANCA binds PR3
Wegener’s granulomatosis

P-ANCA binds Myeloperoxidase
Microscopic polyarteritis
Churg Strauss disease

38
Q

Antiphospholipid Antibodies (Anticardiolipin, Lupus)

A

SLE
Syphilis
Antiphospholipid syndorme

39
Q

Rheumatoid factor

A

IgM that targets IgG

  • Rheumatoid arthritis (50%)
  • Sjogrens
  • Primary Biliary Cirrhosis
  • SLE
  • Subacute Infective Endocarditis
40
Q

HLA disease states

A

DR4 Rheumatoid
DR3 Graves, Diabetes, Dermatitis herpetiformis
DR2 Goodpastures
B27 Ank Spondylitis

41
Q

Type 2 reactions

A

Ab mediated
Ab binds to cell
-Opsonisation
-Classical complement activation

Haem anaemia
BLood transfusion, ITP
Good pastures
Pernicious anaemia
Myasthenia gravis
Graves
Pemphigus
42
Q

Type 3

A

Immune complex deposition

  • SLE
  • Post strep glomerulonephritis
  • Reactive arthritis
  • Serum sickness
  • Arthus reacion
  • Rh arthritis if Rh factor +ve
43
Q

Type 4

A
MS
T1DM
Rheumatoid arthritis
Mantoux test
Contact dermatitis
44
Q

Transplantation rejection

A

Hyperacute-preformed abs

Acute cellular rejection-Type 4 hypersensitivity. Foreign HLA presented. Multicellular response

Acute vascular-Pure antibody reaction-pre-existing antibody or new Ab-intiates complement

Chronic allograft-reaction that causes fibrosis of lumens, scarring and fibrosis