Genetic Factors AP-1, NFAT and NFKB and Immunity. Overview
The activation of the immune response is a complicated subject so I will stick to the basics.
CD4, helper T lymphocytes, and CD8, cytotoxic lymphocytes that kill cancer cells and virally infected cells, are activated in a very precise and controlled manner.
In this essay, we are going to concentrate on two membrane receptors on CD4 and CD8 cells.
The first receptor or receptor complex is called TCR or T cell receptor. This receptor responds to specific antigens, such as cancer or viral proteins. The specificity of this receptor constitutes the genetics of a particular immune response.
The second receptor is called CD28. This receptor binds to membrane receptors on accessory cells such as macrophages and dendritic cells.
Activation of the immune response occurs only in the lymph nodes or spleen. In order for a CD4 or CD8 T cell to become activated, it must physically bind the membrane of an accessory cell. This physical interaction initiates a cascade of biochemical events that results in the activation and growth of lymphocytes.
Both the TCR and CD28 molecules on T cells must be activated at the same time. This activation results in the further activation of genetic factors such as NFAT, AP-1 and NFKB. There are others, but these are the Big Three.
When the CD28 molecule on lymphocytes binds the B7 proteins on the surface of accessory cells, the signaling pathway PI-3k/AKT is activated. The activation of this pathway is critical for maximal immune responsiveness to antigens.
IL-2, one of the most important immune hormones, is activated when its gene binds NFAT, AP-1 and NFKB. The first two are the most important.
If a T lymphocyte specific for a viral protein, for example, is activated by the TCR, BUT if the CD28 signal, mediated by PI-3k/AKT signaling, is blocked, the cell will die of AICD or activation induced cell death. This is very common in HIV infections.
Simply put, we need BOTH TCR and CD28 signaling to be maximally effective in order to mount a vigorous immune response against a pathogen.
In the next essay, I will attempt to explain how melatonin, lithium and a small oxidative stress can maximally activate all three genetic factors previously described.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
(http://www.grouppekurosawa.com)
CD4, helper T lymphocytes, and CD8, cytotoxic lymphocytes that kill cancer cells and virally infected cells, are activated in a very precise and controlled manner.
In this essay, we are going to concentrate on two membrane receptors on CD4 and CD8 cells.
The first receptor or receptor complex is called TCR or T cell receptor. This receptor responds to specific antigens, such as cancer or viral proteins. The specificity of this receptor constitutes the genetics of a particular immune response.
The second receptor is called CD28. This receptor binds to membrane receptors on accessory cells such as macrophages and dendritic cells.
Activation of the immune response occurs only in the lymph nodes or spleen. In order for a CD4 or CD8 T cell to become activated, it must physically bind the membrane of an accessory cell. This physical interaction initiates a cascade of biochemical events that results in the activation and growth of lymphocytes.
Both the TCR and CD28 molecules on T cells must be activated at the same time. This activation results in the further activation of genetic factors such as NFAT, AP-1 and NFKB. There are others, but these are the Big Three.
When the CD28 molecule on lymphocytes binds the B7 proteins on the surface of accessory cells, the signaling pathway PI-3k/AKT is activated. The activation of this pathway is critical for maximal immune responsiveness to antigens.
IL-2, one of the most important immune hormones, is activated when its gene binds NFAT, AP-1 and NFKB. The first two are the most important.
If a T lymphocyte specific for a viral protein, for example, is activated by the TCR, BUT if the CD28 signal, mediated by PI-3k/AKT signaling, is blocked, the cell will die of AICD or activation induced cell death. This is very common in HIV infections.
Simply put, we need BOTH TCR and CD28 signaling to be maximally effective in order to mount a vigorous immune response against a pathogen.
In the next essay, I will attempt to explain how melatonin, lithium and a small oxidative stress can maximally activate all three genetic factors previously described.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
(http://www.grouppekurosawa.com)
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