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MRCOG Part one > Basic Immunology > Flashcards

Basic Immunology Flashcards

1
Q

What are the 2 main categories of the immune system?

A

Innate and adaptive

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2
Q

Explain the differences in

  • resonse time
  • specificity, memory, response to repeat infection, cellular components and humeral components
A

Innate: Response hours, limited specificity, no memory, identical response to repeat infection, phagocytes/NKC, complement pathway

Adaptive: réponse days, diverse specificity, efficient memory, in repeat infection much more rapid and vigorous response, T cells/Bcells, antibodies

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3
Q

What are the main types of phagocytes?

A
  • Monocyte/macrophage lineage

- granulocytes (neutrophils, mast cells, basophils and eosinophils

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4
Q

What is the most abundant type of leukocyte?

A

Neutrophils

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5
Q

How are phagocytes routinely activate?

A

Attracted to chemokine and activate by cytokines that are secreted by antigen specific T cells

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6
Q

How do NK cells detect tumour cells to virally infected cells?

A 
CD16 receptor (FcyRIII) - attaches to specific antibodies bound to tumour cells/virally infected cells
KIRs (killer cell immunoglobulin like receptors) - interacts with MHC class 1 on target cells
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7
Q

Describe the 3 ways in which the complement pathway can be activated (both adaptive & innate.

A
  • Classic pathway (Antigen-antibody complex) adaptive immunity
  • Alternative pathway (C3b bind to hydroxyl/amine group on surface of pathogen) Innate
  • Lectin pathway (lectin binds to glycoproteins + carbohydrates on surface of pathogens)
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8
Q

Briefly describe the complement pathway

A

The most abdundant complement C3 is activated by either of the 3 pathways, all coverage as C5-C9 interact to form a membrane attack complex which binds to the membrane of target cells → transmembrane channel salt & water can flow = lysis

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9
Q

Where are B cells developed?

A

Bone marrow

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10
Q

Briefly describe the activation of B cells

A

Antigens bind to antibodies on the surface of the naive B cells. They are internalised and complex with MHC class II and returned to the cell surface.

Antigen-specific T cells recognise these and secrete cytokines causing clonal B cell proliferation and differentiate into plasma cells which produce antibodies.

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11
Q

What are the 5 main types of antibodies?

A

IgM, IgG, IgA, IgE, IgD

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12
Q

What is the basic structure of antibodies?

A

2 identical light chain
2 Identical heave chains
Differ in size, charges carbohydrate content and amino acid sequence.
Antigen binding fragment (fab) region → antibodies antigen specificity
Fc region → effector function

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13
Q

For IgM describe:

  • % of serum immunglobin pool
  • Shape
  • Role in primary/secondary response?
  • Can it cross the placenta?
  • what is its effector function
A
  • 5-10%
  • pentamer
  • 1st antibody in primary response
  • Can not cross placenta, 1st antibody the newborn baby produces.
  • potent activator of complement pathway due to 4 complement binding pathway
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14
Q

For IgG

  • % of serum immunglobin pool
  • Role in primary/secondary response?
  • Can it cross the placenta?
  • what is its effector function
A
  • 70-80%
  • predominant in Secondary immune responses not primary
  • Can cross into placenta
  • Activate complement and bind to phagocytes
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15
Q

For IgA

  • % of serum immunglobin pool
  • Where is it abundant?
  • Role in primary/secondary response?
  • Can it cross the placenta?
  • what is its effector function
A
  • 10-20%
  • Salivia, tears, mucus, breast milk
  • Important in secondary immune response
  • No but secreted in breast milk important for fetes in first few months of life
  • Induce phagocytosis, prevent attachment to mucosal cells
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16
Q

For IgE

  • High affinicty for which cells
  • what is its effector function
A
  • Mast cells and basophils

- Degranulation release of active mediators, allergic manifestations

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17
Q

How does vaccination improve future secondary responses to infection.

A

As vaccination expose the immune system in an inocus antigen, this produces primary antibody response and leads to generation of long lived antigen specific memory B cells.

Subsequent expose to same pathogen leads to faster more intense secondary response.

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18
Q

T cells recognise antigens through the T cell receptors, what 2 main types of TCRs have been categorised?

A

alpha/beta TCRs - 95% circulating T cells

gamma/delta TCRs - T cells in mucosal surfaces (small intestines, pregnant uterus)

19
Q

Explain the maturation of T cells

A

Generated in bone marrow
matured in thymus
- negative selection if regonise self antigens
- single positive for CD4 or CD8
mature cells leave thymus and travel to secondary lymphoid tissues

20
Q

Describe effector function dependant on CD4/8 group

A 
T helper (Th) cell, CD4 + MHC class II
cytotoxic T (Tc) cell, CD8 + MHC class I
21
Q

CD4 positive T cells can be categorised into Th1 and Th2.

What cytokines do they release and what impact does that have on immunity?

A

Th1 produce IFN-y and IL-2 which activate macrophages and CD8 T cells → cell mediated immunity

Th2 produces IL-4 & IL-5 which activates B cells to produce antibodies → humeral immunity

22
Q

What are the main categories of cytokines?

A 
Interferons 
Interleukins 
Chemokine
Growth factors 
Many overlaps between these groups
23
Q

Main roles of chemokines

A

form concentraction gradient along which circulating leucocytes can imgrate towards the stimulus

24
Q

What are the main groups of Class I MHC.

What is the length of the protein it can present to CD8 positive T cells.

A

HLA A/B/C/E/F

8-9 amino acids

25
Q

What are the main groups of Class II MHC.

What is the length of the protein it can present to CD4 positive T cells.

A

HLA-DR, HLA-DQ, HLA-DP

15-24 amino acids

26
Q 
Describe the terms:
Autograft 
Isograft 
Allograft 
Xenograft
A

Autograft: one part of body to another on same individual
Isograft: transfered betwee genetically identical indvidual
Allogrft genetically different, same species
xenograft different species

27
Q

Describe graft vs host diease

A

The grat initiates a rejection response again recipient
Immune competent T cells from graft recognise MHC or minor histocompatibility as forming and initateimmune response against the host.

28
Q

How to prevent graft vs host

A

careful match of HLA groups
removal of all T cells from the graft
effective immunosuppression

29
Q

Describe 3 main types of graft vs host

A

Hyeracute (mins to hours) natrually occurring antibodies
Acute rejection (days to weeks) donor leukocytes migrate out of graft and initiate primary immune response - Type IV hypersensitivity
Chronic months-years: occlusion of blood vessels, macrophage infiltration and smooth muscle proliferation

30
Q

Explain main features of type 1 hypersensitivity reaction and examples

A
  • Allergen + IgE activate mast cells which release histamine
  • Once mast cells are sensitised on repeat exposures → explosive release of histamine/leukotriene

e.g.: Allergic asthma, anaphylaxis

31
Q

Explain main features of type 2 hypersensitivity reaction and examples

A

IgM + IgG antibodies bind to antigens on cells or extracellular material.
Generally cytotoxic
tissue specific

e.g Haemolytic anaemia (RBCs), good pastures (glomerula membrane) graves TSK receptor, myasthenia graves

32
Q

Explain main features of type 3 hypersensitivity reaction and examples

A

Failure to clear immune complexes, which travel in the blood and are deposited (kindey, joints) - where they activate the complement pathway, attract granulocytes

Examples
Lupus
RA
viral hepatitis 
farmers lung/ pigeon fanciers lung
post strep gloemrular neuritis
33
Q

Explain main features of type 4 hypersensitivity reaction and examples

A

Localised inflammatory reaction caused by T cells at site of antigen, develops over 24-72 hours.

Foreign: Nickle
Autoimmun: IBD, MS, T1DM, hasimatos
GVHD

34
Q

What are the 2 immunological interfaces of pregnancy?

A
  1. Extravillous cytotrophoblst which invades into decide - tissue/tissue
  2. Surface if the chorionic villus (syncytotrphoblast) and maternal blood (gas + nutrient exchange - tissue/blood
    extended 2: syncytiotrophoblast in maternal circulation
35
Q

Which class of MHC does the extravillous cytotrophoblast express?

A 
MHC class 1 ONLY HLA-C/E/G (not A/B)
no MHC class II
36
Q

Which class of MHC does the syncytiotrophoblast express?

A

Neither MHC class 1 or 2

37
Q

What maternal immune cells are found at the interactive between invasive extravillous cytrotrophoblast

A

T cells, macrogphafes, dendritic cells
No B cells
Decidual NK cells (70%) - not cytotoxic, produces cytokines/chemokines/angigenic factors

38
Q

What is unique about HLA-G

A

Very little polymorphism (4 alleys) maternal & paternal likely to be identical and therefore unlike to induce an alloreactive maternal T response during pregnancy

Does not induce immune response but instead implantation, trophoblast invasion and placentation

39
Q

What is the difference of the immune response between the fetal leukocytes that entre the maternal bloods vs extravillous cytotrophoblast/syncytiotrophoblast?

A

Fetal leucocytes express HLA-A HLA-B HLA-C can simulate antoboud mediated and cell mediated immunity

40
Q

Explain the process of haemolytic diease of the newborn

A

RHD- mother has RHD +ve baby. Fetal blood enters maternal circulation, mother produced Anti RhD antibodies + memory B cells post partum. No clinical significant until 2nd pregnancy with Rhesus +ve baby.
IgG crosses placental barrier and damages fetal RBCS → fetal anaemia, impaired platelet function and dysfunction of liver and spleen

41
Q

How is the maturation of CD+ve into Th1 & Th2 changed in pregnancy?

A

Placenta produces Th2 promoting cytokines (IL4 &IL10) + progesterone which inhibitors Th1 response.

Bais to T2 immunity (humoral rather than cellular. Product paternal DNA

42
Q

Affect of shift of T1 on

  • RA
  • Herpes/malria
  • Lupus
A
  • RA is Th1 mediated - temoprary remission
  • Exacerbation of intracellular disease herpes & malaria
  • Worsening of LUPUS (Th2 mediated)
43
Q

What is the incidence of antiphopholipid syndrome in the obstetric population?
What is the risk of fetal mortality?

A

2-5%
85-95%

Consider antiphospholpid if high rates of miscarriage and blood clots

MRCOG Part one (28 decks)

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