Once the barriers have fallen and the non-specific defences overcome, the third line of defence involves special white blood cells, called lymphocytes. The specific immune system recognises the individual pathogens and responds directly to them. It is able to not only tell that the pathogen is foreign, it is able to recognise the specific, individual pathogen. It does this through the surface markers and receptors on the invading cells. Further, it is able to remember these pathogens and respond quicker to future infections.
Lymphocytes, Antigens and Antibodies
The lymphocytes involved in the specific response are T cells and B cells, sometimes called T lymphocytes and B lymphocytes, and they have distinctly different roles in the immune response which will be the main focus of this essay. In very general terms these cells either produce antibodies which bind with antigens and inhibit their function or remember specific antigens and initiate a rapid response to any future invasion.
I’ve just used two terms, antigen and antibody, that I haven’t introduced yet. I’ll give a brief definition that I will expand on later. An antigen is a substance, usually a protein or glycoprotein, that when recognized as non-self by the immune system stimulates the production of an antibody that specifically reacts with it. An antibody is a specific protein produced by animals in response to antigens. Antibodies recognise and bind to the specific antigen that induced its production. Seem a circular definition? Think of it this way. Antigens are receptors on the pathogen that identify it. Antibodies block these receptors stopping it from infecting the host. These are shape specific and I will discuss in more detail in a second. First watch this.
Before I go any further I want to talk about the recognition of self and non-self. This is done via a series of proteins that protrude from the cells membranes and like any receptors shape is extremely important in how they function. We call these Major Histocompatibility (MHC) markers, and these are like an individual’s unique barcode. They come in two varieties MHC Class 1 markers which are found on all cells within the human body except red blood cells, and MHC Class 2 markers which are found on T & B cells and some macrophages along with MHC Class 1 markers. We first came across MHC markers in my essay on pheromones. These are the things you ‘smell’ when assessing the reproductive value of a potential partner. You are attracted to someone who has MHC markers on their pheromones that are most different to your own. Back to immunity, B & T Cells ignore cells with the same MHC markers. It is when MHC markers of a foreign body are recognised that they react.
Antigens receptors on B & T cells that recognise non-self molecules/cells are called immunoglobulins. Immunoglobulins have a specific nature and recognise only one antigen. Like the lock and key of enzymes they are shape specific. During development in the bone marrow variations occur producing literally millions of B cells with different immunoglobulins on the surface. Some of these are genetically encoded, some of these as a result of previous exposure to a pathogen, some as a result of mutation.
Humoral Immunity - B Cells
Develop and mature in the bone marrow. Once mature they leave the marrow and migrate where they are found in the blood, tissue and lymph nodes (lymphatic system will be in one or two essays time). While there may be millions of different types of immunoglobulins on millions of different B cell, the numbers of these individuals are low. For example, there may be millions of B cell but only a handful with a particular receptor. When one of these comes in contact with a specific antigen a series of responses are triggered. The B cell under goes rapid clonal division, it makes many, many copies of itself. These then differentiate into plasma cells that have the role of producing and releasing antibodies into the body’s fluids. The antibodies bind with the antigens on the pathogen preventing it from infecting the body further and making it easier for macrophages to come along and eat them. Some of the B cells become what is called B memory cells and hang around in the blood for years waiting for that pathogen to invade again. Initially, the B cell response to a pathogen is slow due to the fact that they have to undergo clonal division before they can be effective. The presence of B memory cells insures that future infections by this pathogen are responded to much faster.
A response that involves the production of antibodies is called a Humoral Response or Humoral Immunity.
B Lymphocyte rave
B Lymphocyte rave
Cellular Immunity - T Cells and Phagocytes
While Humoral Immunity referred to an immune response involving antibodies and therefore B cell, Cellular Immunity is the term for a response that involves T cells and some phagocytes. Immature T cells leave the bone marrow and move to the thymus where they mature. T cells are the second type of cell involved in specific immunity. When discussing macrophages a blog or two ago I said that they had a role in the specific immune response. When they phagocytise a cell they take the MHC markers from that pathogen and stick them to their own cell wall alongside their MHC Class 1 markers. Like this. Specialised T cells, called T helper cells recognise these foreign class 2 markers on the phagocytes, this causes them to initiate a clonal response and production of antibodies in B cells, not the T cells. They help the B cells respond. In fact this type of B cell only responds to stimulation from a T cell. T Helper cells
Another important type of T cell are the Cytotoxic T cells. Cells infected by a virus display the viral antigen on the surface of the membrane as well as its own MHC markers. The cytotoxic T cell recognises the infected cell by the presence of the foreign antigen and responds by producing proteins that cause holes in the membrane of the infected cell, destroying it.Cytotoxic T cells
Evolution and why we get the flu year after year
To a pathogen living in a Darwinian world, our immune system is a powerful selective pressure. Heritable variations and mutations that provide a pathogen an advantage lead to an evolutionary ‘arms race’ between it and the host. One strategy evolved by viruses, bacteria and protozoans to avoid the body’s defences involves constant change in the three-dimensional structure of these markers on their surface. Regular mutations in the antigen genes create different variant of the MHC markers allowing these pathogens to dodge our immune system – at least over the short term. Our body also produces millions of different variant immunoglobulins on the B cells and some of these can and do match up with the antigens eventually. The problem for us lies in how well these organisms evolve and change. The HIV virus is a master of this. I could spend an hour raving about this one virus. Instead, I’m going to end here after a brief recap.
Recap
- · Specific Immunity involves two main cell types T cells and B cells. Both of these are lymphocytes
- · B cells respond to antigens (receptors) on the pathogen by rapidly cloning themselves and producing antibodies
- · Antibodies bond with the antigens rendering them useless and encouraging phagocytes to come and eat them
- · Some B cells become memory cells so future invasions by the same pathogen are responded to quicker
- · T helper cells recognise foreign MHC marker on the body’s phagocytes after they ingest pathogens. They then kick start the B cells
- · Other T cells called Cytotoxic T cells recognise virus receptors on the surface of infected cells. This causes them to destroy these cells with a protein arsenal
UPDATE: Just noticed I didn't include many of the cells mentioned in non-specific immunity again here as I earlier promised. And I'm not going to. I'm tired and this is more than enough depth for Yr12
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