Antibody Structure and Function 1 of 38 Boardworks
Antibody Structure and Function 1 of 38 © Boardworks Ltd 2008
What are lymphocytes? Lymphocytes are a type of white blood cell (leukocyte) found in the blood and lymph nodes. Lymphocytes recognise antigen molecules on the surface of pathogens, and co-ordinate the immune response against that pathogen. Collectively, lymphocytes can recognize millions of different antigens, due to the large variation of lymphocytes produced. 2 of 38 © Boardworks Ltd 2008
Humoral and Cellular Immune Responses - Involve lymphocytes B-lymphocytes – mature in bone marrow T-lymphocytes – mature in thymus B-lymphocytes produce antibodies – humoral response - T-lymphocytes directly affect cells – cellular response
Different types of lymphocytes 4 of 38 © Boardworks Ltd 2008
Humoral immune response 5 of 38 © Boardworks Ltd 2008
B-cells B-cell binds to antigen. B-cell divides by mitosis. Some cells formed are plasma cells – secrete antibodies. Some cells formed are memory cells – remain in blood for a period of time, providing immunity.
B-cells
Cellular immune response 8 of 38 © Boardworks Ltd 2008
T-cells Phagocyte takes up pathogen. Antigens presented on surface of phagocyte (antigen-presenting cell). T-cell binds to antigen on APC. T-cell divides by mitosis. Several types of T-cell produced, including memory cells and cells that stimulate B-cells to replicate.
T-cells
The graph below shows the levels of anti-Rubella (German Measles) in the blood Concentration of anti-Rubella antibody in the blood/arbitrary units Secondary. BResponse 10000 1000 Primary. AResponse 100 10 10 First exposure X to antigen § infection, or § vaccination 20 30 Long interval Time/days Second Y exposure to antigen
Antibody Concentration – Primary and Secondary Response Primary Response 1. Infection (Ag) 2. Antibodies produced 3. Antibody level rises to combat infection 4. Ag dealt with 5. Ab level declines – short lived Secondary Response After the primary response, Ab’s do not stay in blood – the level declines If the body is infected by the same Ag a second time Ab’s must be made again Re-infection causes much more rapid and a stronger immune response – concentration of Ab’s rises sooner- reaches a higher concentration – more plasma cells than in 1 o response – more cells to respond to Ag; less time to produce same number of plasma cells –hence, a greater [Ab] compared to 1 o response; increased affinity of Ab for Ag. This is due to the presence of memory cells (made during the primary response) – no need for antigen presentation and clonal selection Long-lived; basis of vaccination 12
Primary – establishes immunological memory 13 of 38 13 © Boardworks Ltd 2008
Differences between humoral and cell mediated immunity Humoral Immunity Main cells involved Where do cells develop? Antibodies? How are pathogens identified? How are pathogens killed? How do cells divide once they are stimulated? Cell mediated immunity
Differences between humoral and cell mediated immunity Humoral Immunity Cell mediated immunity Main cells involved B lymphocytes T lymphocytes Where do cells develop? Produced and mature in the Produced in the bone marrow, bone marrow mature in the thymus gland Antibodies? Involves production of antibodies Does not involve production of antibodies How are pathogens identified? Via antigens floating in the blood Via antigens on the surface of infected cells. How are pathogens killed? By antibodies By specialised ‘killer T cells’ How do cells divide once they are stimulated? cells divide into either plasma cells or memory cells divide into different types of specialist T cells
Plasma and memory cells • Plasma cells – – Involved in the primary immune response. Secrete antibodies directly. They only survive for a few days. Response is slow and person will get ill before pathogen is killed. • Memory cells – Involved in the secondary immune response – They circulate in the blood and tissue fluid – When they encounter the antigen from the primary response they divide rapidly. – Response is rapid and person will not get ill.
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