Ch2 Flashcards
1
Q
What are antigens and what are they usually made up of?
What molecules are present with a large amount?
A
- molecules that are recognised by B-cell receptor (antibody) and T-cell receptor
- mostly proteins, carbohydrates and lipids
- with many epitopes
2
Q
What are immunogens?
A
- substances that induce an immune response
- not all antigens are immunogens as recognise is not the same as trigger (eg. self-antigen)
3
Q
What is B-cell receptor and what is its function?
A
- membrane-bound antibody or immunoglobin (Ig) molecules (IgM and IgD isotopes)
- recognise the 3D structure (conformation) of unprocessed antigens
4
Q
What is the structure of B-cell receptor?
A
- Y-shaped with 2 heavy and 2 light chains (include constant Fc and variable Fab regions) joined together by disulphide bonds
- variable heavy and variable light chain –> antigen-binding sites
5
Q
Where can T-cell receptor be found and what is its function?
A
- only found on the surface of T-cell receptor membrane
- only recognise processed peptide antigen fragments displayed on MHC molecules, which bind to CD4 or CD8 co-receptors (CD4 on helper T cells bind to MHC II and CD8 ono cytotoxic T cells bind to MHC I)
6
Q
Why can our immune cells specifically recognise so many different types of antigens?
A
- millions of harmful pathogens –> millions of antigen-binding sites on B-cell and T-cell receptors are required
- diversity is achieved by the rearrangement of gene segments coding for variable domains of B-cell and T-cell receptors during lymphocyte maturation
- heavy chain: V (variable), D (diversity) and J (joining) genes
- λ and κ light chain: V and J genes
7
Q
What is the structure of T-cell receptor?
A
- with 2 polypeptide chains: α and β (with constant and variable regions)
- variable regions of α and β chains –> antigen-binding sites
8
Q
What is the process of acute inflammation?
A
- tissue injury triggers the release of histamine from mast cells –> vasodilation (redness and heat) and increased permeability of blood vessels (swelling and pain)
- blood clotting proteins move from the blood to the tissue –> clotting begins
- increased migration of phagocytes from blood to the injury site
- phagocytes eliminate invading pathogens and cell debris by phagocytosis –> tissue heals
9
Q
What is the role of B cells in antibody production?
A
- B cells circulate in blood and lymph or reside in lymphoid tissues
- respond to T-dependent and T-independent antigens
10
Q
What are T-dependent antigens?
A
- mainly peptide Ag/ protein Ag so most antigens are T-dependent
- require helper T cells which secrete cytokines (eg. interleukin-2) –> stimulate B cells differentiate into plasma cells and memory B –> production of antibody
11
Q
What are T-independent antigens?
A
- mainly polysaccharide or lipopolysaccharide Ag with long repeating units
- bind to many B-cell receptors at the same time –> strong stimulus for B cell to proliferate and differentiate into plasma cells –> Ab production
- no memory B cells –> no secondary immune response
12
Q
What are the functions of antibodies?
A
- Ab bind to and enhance elimination of Ag
- variable regions Fab of Ab –> Ag binding sites
- constant regions of heavy chain –> Ag elimination (as Ab receptor will bind to Fc region)
13
Q
Through what mechanisms can antibodies eliminate Ag?
A
- neutralisation –> Ab attach to microbes –> coat and inactivate bacterial toxins
- agglutination –> Ag are clumped together by antibodies as each Ab has at least 2 Ag-binding sites
- opsonisation –> antibody-bound Ag are more susceptible to phagocytosis as phagocytes have Fc receptor to recognise antibody –> enhance phagocytosis
- complement activation –> complement bind to antibody-coated antigen –> efficient cell lysis –> cells become leaky
- antibody-dependent cell-mediated cytotoxicity (ADCC) –> non-specific cytotoxic cells (eg. neutrophils, macrophages, natural killer cells and eosinophils) bind to Ab-coated Ag via Fc region of Ab –> destroy target cells by lytic enzymes (lysozyme), perforins (pore-forming enzymes) and granzymes (digestive enzymes)
14
Q
What is primary response? What is the process and result of this response?
A
- first exposure to Ag (T-dependent)
- B and T cells are activated and differentiate into plasma cells, helper and cytotoxic T cells and memory B and T cells
- Ab level increases from 10-14 days after exposure to Ag
- IgM predominates over IgG
15
Q
What is secondary response? What cells are involved? What is the process and comparison between primary and secondary response? What is the result of the response?
A
- second exposure to the same Ag –> involves memory B and T cells
- faster (2-7 days), higher titres, more prolonged than primary response
- IgG predominates over IgM
