I'm not going much in-depth here, just kickstarting a discussion. People can post some useful links and discuss to get a better understanding about these cell interactions.
I am wondering, if we can create a knowledgebase on Th1 vs Th2 vs Th17 vs TReg, if anyone has knowledge on this topic, would be so appreciated.
The reason I ask is, there is A LOT of confusion I feel, even in the most expert practitioners as to which are the better pathways.
Prior to Covid, experts used to say: Th2 is anti-inflammatory (IL-10) so better, Th1 is inflammatory. Though now with Covid, we hear the opposite.
@ journey
Boost Th1 response just prior to orgasm. Find stuff that can boost Th1 cytokines, these will block Th2 cytokine release.
Note this discussion is not about their numbers but about their activity. Th1 and Th2 cytokines keep eachother in balance. Th1 cytokines inhibit release of Th2 cytokines which leads to Th1 polarization and vice versa.
Inflammatory cytokines: Increase activity of enzymes (like COX-2) which induce inflammatory symptoms (redness, pain, swelling).
Anti-inflammatory cytokines: Decrease activity of enzymes which induce inflammatory symptoms.
Th1 dominance (polarization):
Pro: resistance against intracellular infections
Con: makes you prone to development of autoimmune diseases.
Th2 dominance (polarization)
Pro: better resistance against extracellular pathogens (bacteria)
Con: susceptible to intracellular infections (viral). It makes you prone to allergic diseases.
Main cytokines that keep Th1/Th2 cytokine release in balance are IFN-g (Th1) and IL-4 (Th2).
IL-10 is the main cytokine of Tregs (with TGF-b). These are anti-inflammatory. The above picture represents a healthy person. If a cell type becomes more active then the plate will get out of balance and gets an angle (not horizontal anymore).
You can read it up in an entry level book about immunology, pick the most basic/elementary book that is available.
So when you have a bacterial infection going on you are likely to produce more Th2 cytokines to fight that pathogen. You will get Th2 polarized which makes you susceptible to allergic diseases. A viral infection will probably lead to Th1 activation and thus to a Th1 dominance of the immune system to fight the virus.
Example 1:
Th1 polarized:
Th2 cytokines are barely detectable. So this person went for autoantibody tests and found Alpha-1 adrenergic receptor and M4 auto antibodies.
Example 2:
Th2 polarized:
IL-4 (Th2) is suppressing IFN-g (Th1) and IL-2 (Th1). IFN-g and IL-2 levels are very low in the above case.
Example 3:
Treg activation
Tregs are able to suppress primarly Th17 cells (and possibly both Th1 and Th2 simultaneously). Tregs form a separate axis with Th17 similar as in the first picture about the Th1/Th2 axis. Tregs are implicated in tolerance to self-antigens (autoimmunity). Treg activation can lead to a suppression of IL-17A. IL-17A is critical in the defense against fungal pathogens (at certain locations inside the body) like Candida Albicans for example. So Treg activation may lead to an heightened susceptibility to fungal infection.
