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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.
If pathogens do invade the body, the subsequent immune response is split between:
The non-specific immune response is inflammation and phagocytosis.
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).
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.
Vaccinations prevent symptoms of an illness (such as flu) from developing, by creating a primary immune response to an unharmful substance that the body identifies as a pathogen. This could be an antigen, or the pathogen itself – dead or otherwise modified to prevent disease. Some vaccines are really successful and have prevented many diseases so far, yet the flu vaccine remains a challenge due to the above points. The virus changes its antigens, and there is great variation to start off with.
There are ethical considerations surrounding vaccination. On the one hand, large scale vaccination can prevent escalation of epidemics via herd immunity. When more people are immune to a certain infectious agent, transmission from person to person becomes more difficult even when a small number of cases do occur.
Therefore, anyone getting vaccinated would want to ensure others follow suit. On the other hand, the personal decision to get vaccinated can interfere with the goal of achieving a good immunity status for a given population against an illness. Some people would be cautious to get themselves or their children vaccinated due to suspected long term side effects.
The balance of personal autonomy versus achieving greater societal goals that require everyone to synchronise in their decision making has to be accomplished.
Active immunity refers to immunity acquired as a result of an illness. This is also the type of immunity induced via vaccination, as the body is responding in the same way when it encounters the pathogenic antigen and responds appropriately.
Passive immunity is the type of immunity acquired directly via the relevant antibodies rather than by developing them afresh following disease or other ways of contacting antigens. An example is the immunity passed to a foetus via the placenta during gestation.
HIV and AIDS
The human immunodeficiency virus causes acquired immune deficiency syndrome. Upon infection, it replicates in helper T cells. HIV is a lentivirus with the expected viral components such as its genetic material (RNA in this case) and capsid.
Upon infection via transmission of infected bodily fluids such as blood or semen, the virus seeks its host cell, the helper T cell which is a key component of the immune response. As HIV hijacks the cell’s machinery to replicate, it destroys it and thus impedes the immune response, leaving the victim with a compromised immunity and therefore susceptible to opportunistic infections.
Part of the HIV replication strategy is the embedding of its genetic material into the host cell’s DNA. The virus contains RNA which has to first be converted into DNA. This is what the reverse transcriptase enzyme does (transcription is DNA to RNA, so reverse transcription is RNA to DNA).
Some drugs for AIDS take advantage of this DNA embedding step by preventing it, and therefore slowing down the replication process of the virus. The reason antibiotics don’t work on any viruses is quite simple. We’ve seen that prokaryotes like bacteria are a cell of their own with many different structures and organelles such as a cell wall, while viruses are neither a cell nor alive. You can imagine you can’t really target something as vague as a piece of genetic information in a protein capsid.
Bacteria have complex cell walls with many components and various enzymes building them up or performing other metabolic functions within the cell. Any of these parts or processes can be targeted, as long as it is distinct from its host (that is ourselves with our eukaryotic cells that do not, for example, have cell walls and thus won’t be harmed by the antibiotic if that’s the part it targets). Viruses have no cell walls, no ribosomes, nothing really taking place.
These are antibodies which can be cloned from a single cell to make a high amount of them. They can bind to pretty much any substance, and are used in pregnancy tests as well as cancer treatment.The process involves taking a cell which produces antibodies such as a lymphocyte, and crossing it with a tumour cell. Tumour cells divide uncontrollably, so the end hybrid cell will produce many antibodies via its many clones.
The antibodies are also used to customise drugs to make them target specific cell types, as well as in medical diagnosis. This is often done via a basic detection technique called ELISA (enzyme-linked immunosorbent assay). It takes advantage of the antigen-antibody specificity to produce a signal by attaching an enzyme to the antibody and adding its substrate. If the antibody binds to the antigen in the sample, the enzyme attached to it reacts with the substrate to produce the signal, often a colour change. This indicates the presence of the antigen that the specific antibody has an affinity for. Sometimes both primary and secondary antibodies are used in sequence.
The extent of colour change can be quantified using a spectrophotometer. This reads the absorbance of light passed through the sample of coloured liquid. This varies finely according to the colour and can be obtained at specific wavelengths (green light, red light, etc.).
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