Adaptive Immune Response (HL IB Biology)

• Every organism has cells with unique molecules on the cell surface membrane which act as markers to identify it
• These unique markers are macromolecules and they allow cell-to-cell recognition
• The immune system has the ability to distinguish between 'self' and 'non-self' based on these molecules
  • Microorganisms (both pathogenic and non-pathogenic), such as bacteria and viruses, trigger an immune response as the immune system recognises their markers as being non-self 
  • Molecules that trigger an immune response in this way are named antigens
  • Antigens are found on cell surface membranes of cancer cells, bacterial cell walls, the envelopes of viruses and even pollen grains
  • Some glycolipids and glycoproteins on the outer surface of cell surface membranes act as antigens
• Allergies are the result of an immune response triggered by antigens on the surface of an allergen, such as pollen

Antigens on red blood cells

• Red blood cells have specific markers on their surface known as antigens which determine the blood group of an individual
• If a transfusion is given to an individual with mismatched blood group, the antigens on the red blood cell surface will trigger an immune response
• There are two antigen markers that must be considered:
  • The ABO marker - this determines whether the individual is blood group A, B, AB or O
  • The Rhesus (Rh) marker - this determines whether the individual is rhesus positive or rhesus negative

Determining ABO blood types

• Blood type A has a type A antigen consisting of an initial 'H' marker which is modified with another molecule called N-acetylgalactosamine
• Blood type B has a type B antigen consisting of an initial 'H' marker which is modified with another molecule called galactose
• Blood type AB has type A and B antigens consisting of two 'H' markers one of which is modified with N-acetylgalactosamine and the other with galactose'
• In blood type O, the 'H' marker is not modified and so there are no A or B antigens

Antigens and blood type diagram

Blood type is determined by the presence or absence of specific antigen markers on the surface of the red blood cells

• If a transfusion is given to someone of an incompatible blood type, an immune response will occur due to the presence of antibodies in the recipient's blood that bind to blood cells with non-self antigens
• An immune response may result in agglutination of the blood in the blood vessels and could be fatal
  • Agglutination is when red blood cells clump together due to the binding of antigens and antibodies
• Blood type must be compatible when carrying out a transfusion to prevent coagulation of blood in blood vessels

Blood type compatibility table

• T-Helper cells (a type of lymphocyte that responds to specific antigens) and mature B cells (another type of lymphocyte) have specific receptors located on their cell surface membranes
  • These receptors have a similar structure to antibodies and are each specific to one antigen
  • Note that lymphocytes are a type of white blood cell involved in the specific immune response; there are several different types of lymphocyte
• When phagocytes engulf pathogens, they present the pathogen antigens on their own cell surface membrane
  • A cell with non-self antigens on its surface membrane is known as an antigen presenting cell
• The T-helper cell with the complementary receptor proteins to the antigen will bind to the antigen and become activated by the phagocyte
• Activated T-helper cells then bind with complementary receptors on the surface membrane of specific B-lymphocytes
• On binding, the T-helper cells releases signalling proteins and activate these B-cells
• Once activated, the B cells clone themselves to become
  • plasma cells which produce antibodies
  • memory cells which provide immunity against future infection from the same pathogen

B cell activation diagram

Antigens activate complementary T-helper cells which go on to activate complementary B-cells

• Once the B cell has been activated, clonal expansion can then occur
  • The activated B-cell divides by mitosis to create many clones of itself
    • Each clone will produce the exact same antibody, complementary to the target antigen
• Some of these mature B-lymphocytes differentiate into plasma cells 
• The other B-lymphocytes become memory cells that  remain and circulate in the blood
  • Whilst the antibodies produced by the plasma cells are only present for a matter of weeks or months, memory cells form the basis of immunological memory – the cells can last for many years and often a lifetime

• Immunity is initiated when exposure to a specific antigen results in the production of complementary antibodies and memory cells
• This first exposure to an antigen triggers the primary immune response
• The primary immune response leads to the development of immunity if memory cells and antibodies persist in the bloodstream after the pathogen has been eliminated
• The secondary immune response occurs when the same antigen is found in the body a second time
  • The memory cells recognise the antigen, divide very quickly and differentiate into antibody-producing plasma cells and more memory cells
  • The response to a previously encountered pathogen is, relative to the primary immune response, extremely fast
  • This means that the infection can be destroyed and removed before the pathogen population increases too much and symptoms of the disease develop

Developing immunity diagram

During a secondary immune response, memory cells that remained in the blood divide very quickly into plasma cells (to produce antibodies) and more memory cells; 2000 antibodies can be produced per second! Whereas a primary response occurs much more slowly.

Primary and secondary immune response graph

The secondary response is much larger and more rapid than the primary response