Cell Recognition

Cells are labelled with proteins to allow recognition. To prevent your lymphocytes from destroying your own body cells, each of your body cells is labelled a unique shape protein that your lymphocytes recognise as ‘self’ cells. Any other type of protein detected on the surface of a cell is recognised as ‘non-self’ and is destroyed. This could range from abnormal body cells such as cancer, toxins produced by pathogens, pathogens and cells from other organisms of the same species.

An antigen is typically a protein molecule on the cell-surface of a membrane of non-self cells. The presence of antigens triggers an immune response and the production of antibodies.

Response to Pathogens

The first line of defence to prevent infection are physical and chemical barriers, such as the skin and stomach acid. If pathogens get past these barriers then two key types of blood cells respond, the phagocytes and the lymphocytes.

Immunity, figure 1


The phagocytes, such as macrophages and neutrophils, travel in the blood and squeeze out of capillaries to engulf and digest pathogens. This phagocytosis and it is non-specific. Damaged cells and pathogens release chemicals that attract the phagocytes to the site of infection.

Phagocytes have receptors which can attach onto chemicals on the surface of pathogens. The phagocyte then engulfs the pathogen into a vesicle to create a phagosome. Within the phagocyte there are lysosomes which contain hydrolytic lysozyme enzymes.

The lysosome fuses with the phagosome to expose the pathogen to the lysozyme. This hydrolyses the pathogen and any soluble useful molecules are absorbed into the cytoplasm of the phagocyte.

The phagocytes will present the antigen of the digested pathogen on their surface, they are then called antigen-presenting cells.

Immunity, figure 1


The lymphocytes are part of the specific response to antigens. There are two types: B lymphocytes (B Cells) and T lymphocytes (T cells). Both are created by bone marrow stem cells, but B cells mature in the bone marrow where as T cells mature in the thymus.

Cell-Mediated Response

This is the response of T cells to a foreign antigen. Receptors on the T cells will bind onto the antigens on antigen-presenting cells and cause the T cell to divide rapidly by mitosis (clonal expansion). These cloned T cells can then differentiate into different specialised T cells:

  • Memory T cells to enable a rapid response to reinfection of the same pathogen.
  • Cytotoxic T cells kill abnormal cells and infected body cells. They release a protein called perforin which create pores (holes) in the cell membrane. This allows all substances to move into the cell and causes cell death.
  • Helper T cells stimulate B cells to divide and secrete antibodies.
  • T cells also stimulate phagocytosis of pathogens.

Immunity, figure 1

Humoral Response

Helper T cells stimulate the B cells and initiate the humoral response, which involves antibodies. Antibodies are proteins that have binding sites complementary in shape to antigens. The binding site is described as the variable region, as the shape changes for each antigen. The rest of the antibody is the constant region. They are made up of four polypeptide chains, two heavy and two light chains. When an antigen binds to an antibody it is described as an antigen-antibody complex.

Immunity, figure 1

Immunity, figure 2

Antibodies help destroy pathogens by either causing agglutination of marking. Agglutination is clumping together all the bacterial cells, so it is easier for phagocytes to locate and engulf. They also act as markers to stimulate phagocytes to engulf the cells.

Immunity, figure 3

B cells can also become antigen-presenting cells and when these or the helper T cells stimulate the B cells, they B cells rapidly divide by mitosis to make clones. The clones differentiate into either memory B cells or plasma cells. The plasma cells produce antibodies specific in shape to the antigen that initiated the response. The antibodies attach to the antigens on the pathogen to help destroy them by agglutination and marking them to phagocytes. The memory B cells can rapidly produce large amounts of antibodies if there is reinfection of the same pathogen. This is how B cells can provide long-term immunity.

Immunity, figure 4

The first exposure to a pathogen is described as the primary response. It can take a few days for the lymphocytes to create enough complementary antibodies to help destroy the pathogen, so you are likely to suffer symptoms before the pathogen is destroyed. A secondary immune response is when you are re-infected with the same pathogen, but the memory cells can help produce large amounts of antibodies rapidly so the pathogen is destroyed before causing any symptoms. This would be natural active immunity.

Immunity, figure 5

A vaccine can be either passive or artificial active immunity. Passive immunity is when antibodies are injected directly into you to help destroy the pathogen. Artificial active immunity is when antigens or small amounts attenuated pathogen are injected or taken orally. These trigger a primary response but with few symptoms. Therefore, if you are re-infected with the same pathogen you will rapidly produce antibodies as it is the secondary response. In this way vaccines provide protection for individuals and populations against disease. If a large enough proportion of a population are vaccinated, then herd immunity arises. The idea is that if most of the population is immune, it is unlikely that a susceptible individual will encounter an infected individual. Vaccines are not always effective long term though because pathogens mutate, and this could result in their antigen changing shape, this is called antigen variability. Influenza mutates rapidly, and therefore there is a new flu vaccine annually.

Monoclonal Antibodies

A monoclonal antibody is a single type of antibody that can be isolated and cloned. This is used for targeting medication to specific cell types by attaching a therapeutic drug to an antibody and medical diagnosis. Creating monoclonal antibodies requires mice to produce the antibodies and tumour cells, which leads to ethical debates as to whether this use of animals is justified to enable the better treatment of cancers in humans and to detect disease.

Immunity, figure 1

Immunity, figure 2


The human immunodeficiency virus (HIV) structure can be seen below:

Immunity, figure 1

Following infection, the HIV is transported around in the blood until it attaches to a CD4 protein on the helper T cells. The HIV protein capsule then fuses with the helper T cell membrane, enabling the RNA and enzymes from HIV to enter. The HIV enzyme reverse transcriptase copies the viral RNA into a DNA copy and moved to the helper T cell nucleus, this is why it is called a retrovirus. Here mRNA is transcribed, and the helper T cell starts to create viral proteins to make new viral particles.

Immunity, figure 2

HIV positive is when a person is infected with HIV, but it is only when the replicating viruses in the helper T cells interfere with their normal functioning of the immune system that symptoms develop, resulting in AIDS. With the helper T cells being destroyed by the virus, the host is unable to produce an adequate immune response to other pathogens and is let vulnerable to infections and cancer. It is this destruction of the immune system that leads to death, rather than the HIV directly.

What is an antibody?
Your answer should include: Protein / complementary / shape / antigens
What is a monoclonal antibody?
Which lymphocytes stimulate both the cell-mediated and humoral response?
Your answer should include: T / cells
Which cells create antibodies?
Your answer should include: plasma / cells
Explain why HIV is called a retrovirus:
Your answer should include: reverse / transcriptase
What is the difference between HIV and AIDS?
Your answer should include: virus / result