Innate immune cells and their role in immunity

Question 1

What is meant by antigen presentation?

Answer 1

1. During phagocytosis proteins broken
   down to peptides
2. Peptides displayed on the surface
3. Present Peptides to T cells
4. Inform T cells what pathogen was detected

Question 2

What are the two antigen presenting receptors?

Answer 2

1. MHC 1:
   - MHC class I found on all nucleated cells
   - Presents material from self/tumour or intracellular
   viruses/bacteria
   - MHC class I is up regulated during infection
   - Presents to CD8 T cells
2. MHC 2:
   - MHC class II found on antigen presenting cells – macrophages, dendritic cells and B cells
   - Presents material from endocytosed/phagocytosed
   bacteria/viruses
   - Up regulated when APCs activated
   - Presents to CD4 T cells

Question 3

What are the principles behind MHC diversity?

Answer 3

1. HLA genes are the most polygenic and polymorphic in human population
2. Therefore each individual has a unique set of MHC (MHC haplotype)

3.Different MHC molecules bind different peptides

4. MHC 1 (A,B,C) AND MHC 2 (DP, DQ, DR)
5. Humans will select a partner with a different MHC repertoire – ensures genetic diversity (olfaction & pheromone peptides)

Question 4

What is the role of MHC in graft rejection?

Answer 4

1. MHC class I is found on all nucleated cells and marks your own cells as ‘self’
2. T cells have evolved to recognise self-MHC and will not attack
3. In graft rejection, recipient T cells will not recognise non-self MHC and destroy donor cells and raise antibodies to non-self MHC
4. Prevention is reduced by HLA typing individuals and immunosuppressive drugs

Question 5

What is the complement system and what is its role?

Answer 5

1. It is a collection of circulating and membrane associated proteins
2. It is initiated baby 3 different pathways:
   -Inflammatory response: C3a & C5a proteins promote an inflammatory response. Mast cells are degranulated, causing ^ vascular permeability.
   - Opsonisation: C3b is left on the microbial cell wall and is recognised by phagocytes receptors who phagocytose microbe.
   - Lysis: C3b activates C5b which binds to C6-C9 which causes C9 to polymerise and form membrane attack complex. Loss of cell integrity where water and ions enter causing death of certain microbes
3. it is regulated by C1 inhibitors (plasma proteins) which prevents assembly of C1 complex

Question 6

What are the diseases associated with complement disorders?

Answer 6

1. C3 Deficiency is linked with frequent pyogenic (pus-forming) infection in infants and young children and severe pyogenic bacterial infections in adults.
2. Deficiency in some early components (eg C2 and C4) are associated with an increase of immune complex-mediated autoimmune disease (eg systemic
   lupus erythematosus)
3. Deficiency in terminal pathway (C5-C9): The lack of MAC formation results in severe recurrent infections by Neisseria gonorrhoea or Neisseria meningitidis.
4. Deficiency in C1 INH causes a disease called hereditary angioedema