Different cells have different molecules presented on their surface to the immune system. These are often protein-based and enable the identification of:
-cells from other organisms of the same species
-abnormal body cells
The specific immune response is split into humoral immunity and cell-mediated immunity. Humoral is to do with the blood and antibodies. Distinguishing between an antigen and an antibody is very important.
Antigen = protein or carbohydrate foreign (not normally present) to a host’s organism
Antibody = protein made as a response to detecting an antigen which binds to the antigen and prevents the pathogen from harming the host.
Immunity against invading pathogens is a crucial part of maintaining health. The body has adaptations which prevent invasion by pathogens, as well as processes in place to deal with those that manage to penetrate the body’s primary defenses. The skin and mucous membranes (e.g. mouth) are examples of such defenses. Sweat contains lysozyme which is an enzyme that breaks down bacterial walls. The skin flora is made up of all the microorganisms that live on the skin without causing disease. They populate the surface of the body, so invading pathogens can be stopped in their tracks by the resident flora.
Connective tissue, tears, mucus and ciliated epithelium also help protect against infection. Connective tissue forms during scarring and alongside blood clotting, it maintains the barrier against infection. Tears and mucus contain digestive enzymes that maintain eye and respiratory system health by disintegrating microorganisms and keeping a hostile environment to prevent infection. Ciliated epithelium has hair-like protrusions that wave to move out particles that are inhaled for example. They also act in response to these particles by triggering sneezing.
Localised inflammation is also a first response to infection or other types of assaults. Its purpose is to remove the infectious agent and encourage tissue repair. It achieves this by swelling the area with blood containing phagocytes and molecules involved in the immune response such as cytokines.
If pathogens do invade the body, the subsequent immune response is split between:
The non-specific immune response is inflammation and phagocytosis. The specific immune response involves the formation of memory following an infection, in order to better fight and prevent recurrent infections by the same agent that is highly specifically identified.
Neutrophils are the most abundant white blood cell that identifies foreign agents in the body and digests them by phagocytosis. Macrophages are present in tissue and have a similar phagocytic function, but additionally present fragments of the invading agent as antigens to the type of lymphocyte (T cell) that requires this information to identify the invader and mount a specific response against it.
All these cells are able to produce small proteins called cytokines that act in cell signalling to bridge the cell-mediated and humoral responses and regulate the action of all the different cells available.
Antibodies are made by B cells or T cells which come from stem cells from bone marrow. B cells release antibodies, while T cells secrete antibodies which stay on the surface of the cell. Helper T cells stimulate cytotoxic T cells, B cells and phagocytes.
B cell –> O – – – – – –
T cell –> O-
where “–” is an antibody. Apologies for the horrendous visual representation.
So when a bacterium invades, B cells would release antibodies with a shape complementary to that of the bacterium’s antigen. This antibody would then bind to the antigen. T cells on the other hand would secrete the antibodies on their surface, then personally greet the bacterium and bind to it via the antibody. You could say the B cell is shooting the bacterium, while the T cell is strangling it. But for goodness’ sake, don’t write that in the exam.
When a pathogen invades the body and a B cell releases the appropriate antibody to manage the infection, it’s not just the one B cell. They come in their thousands, they are clones of a B cell with a specific antibody, and they are called plasma cells. Plasma cells release a high amount of antibodies, but they are short-lived. Other cells called memory cells may survive for much longer, up to several years. Memory cells are involved in the secondary immune response which happens if a high enough amount of antigens are present. The memory cells replicate into a large number of plasma cells which then release enough antibodies.
OK, so if we have all these fancy cells doing our work for us, how come the cold virus gets us again and again and again? Surely our memory cells could identify the cold virus, replicate and defeat it?
Memory cells are specific to certain antigens. The flu virus has many different variations of antigens which change constantly, so by the time we’ve acquired some resistance to this year’s antigen, a new one will have emerged.
The response not dependent on antibodies involves all the aforementioned phagocytosis-inducing cells like macrophages and neutrophils, as well as cytotoxic T-lymphocytes and the cytokine response to invaders.
White cells (the most common ones are neutrophils) engulf any foreign particles such as dust or bacteria, then digest them and dispose off of the remains. It’s badass, trust me. I’ve got proof:
The enzymes used to break invaders down are lysosomes which fuse with the vesicle which contains the bacteria. All this action happens within the white cell. At the end, the undigested leftovers are disposed off of by exocytosis (kind of like a burp).
T killer cells (a.k.a. cytotoxic) recognise their target and release toxic chemicals to kill them.
The blue cell in the centre is a tumour cell, while the surrounding cells are killer T cells about to release their toxic cargo found in the vesicles stained red. Bye-bye, tumour cell.