Hey guys. SAC 5 is an annotated poster and there are just some topics I want to clarify before I actually start this SAC (annotated posters). I'll put down my understanding and then ask questions relating to some confusion I have regarding a particular topic. Could you please make any necessary amendments.
'Self' materials refers to all matter that belongs to the body cells of the host organism, whilst any 'non-self' materials refers to all matter that is foreign to the host organism and does not belong to the body cells of the organism. The immune system is able to distinguish between 'self' and 'non-self' material in order to defend the organism from any pathogenic agents. The ability to do so originates from the complex of genes found on chromosome 6 of all human cells. These set of genes called the Major Incompatibility Complex code for Class I and Class II MHC markers:
- Class I MHC Markers - these markers are found on the surface of all nucleated, human cells (i.e. except erthythrocytes - red blood cells)
- Class II MHC Markers - these markers are found on the surface of B-lymphocytes, T-lymphocytes and macrophages.
A macrophage is a 'big eater' - a white blood cell that develops from a monocyte. On the surface of macrophages are 'self' receptors; as the name suggests, these receptors have a reception site complementary to the site of the Class I MHC markers of somatic cells of living organisms. If there is a complementary fit between the self-receptor and the MHC class I marker, the macrophage is able to identify it as 'self'. However, if there is no self receptor - MHC class-1 complex formed, the macrophage detects that the antigen (i.e. any substance that triggers an immune response) is foreign, and an immune response is initiated.
The macrophage binds to, engulfs and destroys the foreign, 'non-self' antigen; it releases digestive enzymes packaged in lysosomes, which break down the antigen and digest any material, voiding all the other material that is not required by the macrophage out of the cell. Antigen fragments are collected by Class-2 MHC markers, which migrate to the surface of these macrophages. The whole macrophage then travels to lymph notes, where the process of attracting a T-helper Cell is at a higher chance of occurring. The macrophage secretes the cytokine Interleukin-1, which attracts Helper-T cells; the CD4 receptors on the helper T-cells form a complementary complex with the MHC- Class 2 markers of the macrophage. Then, the helper-T cells secrete Interleukin-2 (cytokine) which aids in the activation of a humoral and cell-mediated immune response.
The humoral response:
B-lymphocytes which produce antibodies specifically designed against the antigen begin to replicate and increase rapidly in number (clonal expansion and proliferation). As the proliferation of B-lymphocytes with specific immunoglobulins occurs (i.e. clonal expansion), some differentiate into plasma cells while others differentiate into memory-B cells. The plasma cells that are produced by the proliferation of B-lymphocytes are involved in the production of specific immunoglobulins (antibodies) against a specific type of pathogen. These antibodies are proteins with a Quaternary structure that bind to specific antigens at the antigen-binding site of the antibody. These antibodies are involved in the agglutination of non-self antigens; that is, these antibodies almost neutralize the actions of the antigens in that they are unable to enter and infect cells of the host. They can also clog all the antigens together and make them more noticeable for macrophages, which then bind to, engulf and destroy these foreign antigens. Furthermore, memory-B cells retain memory of the foreign antigen, and so following the primary antibody response (i.e. the secondary antibody response), the presence of memory-B cells means that B-lymphocytes that produce specific antibodies against the specific antigen will be produced at a greater concentration at a greater rate per unit time, resulting in a more rapid response to the secondary infection by the same pathogen.
Cell-mediated response:
* There are 4 main types of T-lymphocytes that are involved in cell-mediated immunity:
- Helper T~cells
- Cytotoxic T~cells
- Suppressor T~cells
- Memory T~cells
Helper T-cells:
* When a macrophage's Class-2 MHC markers present antigen-fragments on the cell surface, Interleukin-1 is secreted by the cell to attract Helper-T cells. The CD4 receptors of the T-helper cells binds to the Class-2 MHC markers of the macrophage, enabling the activation of the Helper T-cells.
* Helper T Cells are very important because they aid the initiation of a specific immune response to a particular pathogen, leading to a humoral and/or cell-mediated immune response.
Cytotoxic T-cells:
*When a viral-infected cell is detected by a cytotoxic T-cell (i.e. viruses are obligate intracellular pathogens), the class I MHC markers present antigen fragments of the virus to the cytotoxic T-cells. These cytotoxic T-cells' CD8 receptors bind to the class I MHC marker; this then triggers the release of perforin, the protein that punches holes in the cell membrane of the viral-infected cell, inducing its lysis.
* Interferon is simultaneously secreted by this viral-infected cell to make viral-infected cells in the intermediate vicinity more resistant to the virus, in the event that the cell lyses and the viruses escape to move around to potentially infect other cells. The interferon acts on cells to produce an enzyme that prevents viruses from being able to reproduce and grown within the cells.
Suppressor T-cells:
* Suppressor T-cells are involved in regulating the length of time an immune response is initiated for before the immune response to that pathogen is ended.
* Suppressor T-cells multiply very slowly in contrast to helper-T cells and cytotoxic-T cells; this is because it is vital that the non-self antigen is destroyed by the immune response terminates.
Memory T-cells:
* Memory T-cells retain memory about the antigen that has caused infection in cells of the organism, and so next time an infection occurs with the same antigen, the cell-mediated response to destroy the pathogen is done more rapidly than that of the first time the organism had been exposed to the antigen (i.e. primary infection).
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First Line of Defense:
* Non-specific line of defense
* Is intended to prevent the penetration of any pathogenic agents into the internal environment of a living organism.
Intact (kerotinised) skin:
- Cells are packaged tightly together to form a tough, waterproof layer.
- Lined with natural flora that compete with pathogenic agents for nutrients/space ~ benefit the organism.
Ciliated respiratory tract:
-> The presence of fine hair-like projections along the respiratory tract prevents the entry of pathogenic agents.
-> The rhythmic beating of the cilia on the surface of the respiratory tract sends the pathogen upwards towards the nose and mouth.
Acid/Base Environments:
* Many pathogenic agents cannot withstand the severe pH change from the acidic environment of the stomach to the alkaline environment of the small intestine.
Mucus membranes:
- Mucus clogs the pathogenic agents and brings the mucus up to the nose and the mouth to be released from the body.
Tears:
- Lysosymes in tears break down the cell membrane of cellular pathogens.
- These enzymes break down the pathogenic agent, inhibiting its ability to cross the first line of defense.
In plants:
- Epidermis prevents movement of pathogens into the plant.
- Bark.
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Second Line of Defense:
When a pathogen has penetrated the internal environment of a living organism (i.e. bypassed the first line of defense), a series of responses to this pathogen attempt to destroy the pathogen.
Phagocytes:Phagocytes are white blood cells that bind to, engulf and destroy foreign, 'non-self' materials.
Interferon:Interferon is a protein that is released by viral-infected cells. The secretion of interferon acts on the neighbouring cells in the intermediate vicinity, to make them more resistant to the virus by producing enzymes that inhibit the growth and multiplication of the virus, which is an obligate, intracellular pathogen.
Complement Proteins: Complement proteins refer to an array of proteins that are involved in:
(a) Coat pathogenic agents in a substance that makes them more noticeable and obvious to phagocytes.
(b) Involved in breaking the cell membrane of cellular pathogens, resulting in them being broken down; the remnants are then engulfed by phagocytes.
(c) Activate phagocytes.
Inflammation:
1) When the skin has been broken by a cut for example, histamine is released by the tissue that has been damaged, resulting in an increased blood flow to the area.
2) The increased blood flow is created by the release of histamine by mast cells, which causes the dilation of arterioles, resulting in increased blood flow to the affected area.
3) Platelets (cell fragments) form a scab; thus, there can be an increase in the amount of blood that flows to the area, carry phagocytes to engulf any matter that is foreign 'non-self', without too much blood being lost.
I'll be adding more later as I keep on learning more info; thanks for having the patience!! Any constructive criticism can be much appreciated.
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