Hormones can act as immunomodulators, altering the sensitivity of the immune system. For example, female sex hormones are known immunostimulators of both adaptive[95] and innate immune responses.[96] Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty. By contrast, male sex hormones such as testosterone seem to be immunosuppressive.[97] Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D.[98][99]
When a T-cell encounters a foreign pathogen, it extends a vitamin D receptor. This is essentially a signaling device that allows the T-cell to bind to the active form of vitamin D, the steroid hormone calcitriol. T-cells have a symbiotic relationship with vitamin D. Not only does the T-cell extend a vitamin D receptor, in essence asking to bind to the steroid hormone version of vitamin D, calcitriol, but the T-cell expresses the gene CYP27B1, which is the gene responsible for converting the pre-hormone version of vitamin D, calcidiol into the steroid hormone version, calcitriol. Only after binding to calcitriol can T-cells perform their intended function. Other immune system cells that are known to express CYP27B1 and thus activate vitamin D calcidiol, are dendritic cells, keratinocytes and macrophages.[100][101]
It is conjectured that a progressive decline in hormone levels with age is partially responsible for weakened immune responses in aging individuals.[102] Conversely, some hormones are regulated by the immune system, notably thyroid hormone activity.[103] The age-related decline in immune function is also related to dropping vitamin D levels in the elderly. As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels. This means that they get less sun and therefore produce less cholecalciferol via UVB radiation. Second, as a person ages the skin becomes less adept at producing vitamin D.[104]
The immune system is affected by sleep and rest,[105] and sleep deprivation is detrimental to immune function.[106] Complex feedback loops involving cytokines, such as interleukin-1 and tumor necrosis factor-α produced in response to infection, appear to also play a role in the regulation of non-rapid eye movement (REM) sleep.[107] Thus the immune response to infection may result in changes to the sleep cycle, including an increase in slow-wave sleep relative to REM sleep
Wow…This makes a lot of sense. Could it be why our junk shrivillved up because of an anti-inflamatory response. My Junk is up and down is ain’t permanant. Though every has low vitamin D. This explains alot. Not saying this is right. I want to try this.
"Effects of the inflammatory response.
The primary physical effect of the inflammatory response is for blood circulation to increase around the infected area. In particular, the blood vessels around the site of inflammation dilate, permitting increased blood flow to the area. Gaps appear in the cell walls surrounding the infected area, allowing the larger cells of the blood, i.e. the immune cells, to pass. As a result of the increased blood flow, the immune presence is strengthened. All of the different types of cells that constitute the immune system congregate at the site of inflammation, along with a large supply of proteins, which fuel the immune response. There is an increase in body heat, which can itself have an anti-biotic effect, swinging the balance of chemical reactions in favour of the host. The main symptoms of the inflammatory response are as follows.
The tissues in the area are red and warm, as a result of the large amount of blood reaching the site.
The tissues in the area are swollen, again due to the increased amount of blood and proteins that are present.
The area is painful, due the expansion of tissues, causing mechanical pressure on nerve cells, and also due to the presence of pain mediators.
Once the inflammatory process has begun, it continues until the infection that caused it has been eradicated. Phagocytes continue to consume and destroy bacteria, the acquired immune system binds and disposes of harmful toxins. Pus is produced, pus being the debris that is left over from the battle between the invader and the immune system. The colour of the pus depends on the organism causing the infection.
How does the inflammatory response end?
Ideally, the inflammatory response should only last for as long as the infection exists. Once the threat of infection has passed, the area should return to normal existence.
The actual process by which the inflammatory response ends is now only beginning to be understood. The key element is a phenomenon known as “Apoptosis”.
When cells of the body die in a normal fashion, e.g. by being irreparably damaged or by being deprived of nutrients, this is known as Necrotic death. Recently, research has shown that cells can also be killed in another way, i.e. by “committing suicide”. On receipt of a certain chemical signal, most cells of the body can destroy themselves. This is known as Apoptotic death. There are two main ways in which cells can commit Apoptosis.
By receiving an Apoptosis signal. When an chemical signal is received that indicates that the cell should kill itself, it does so.
By not receiving a “stay-alive” signal. Certain cells, once they reach an activated state, are primed to kill themselves automatically within a certain period of time, i.e. to commit Apoptosis, unless instructed otherwise. However, there may be other cells that supply them with a “stay-alive” signal, which delays the Apoptosis of the cell. It is only when the primed cell stops receiving this “stay-alive” signal that it kills itself.
The immune system employs method two above. The immune cells involved in the inflammatory response, once they become activated, are primed to commit Apoptosis. Helper T cells emit a stay-alive signal, and keep emitting that signal for as long as they recognise foreign antigens in the body, prolonging the inflammatory response. It is only when the infection has been eradicated, and there is no more foreign antigen that the helper T cells stop emitting the stay-alive signal, thus allowing the cells involved in the inflammatory response to die off.
If foreign antigen is not eradicated from the body, or the helper T cells do not recognise that fact, or if the immune cells receive the stay-alive signal from another source, then chronic inflammation may develop."
