About the author : victoriafenton

One of my regular discussions with educated clients is about Th1 and Th2 dominance.  It’s another one of those things (like “Adrenal Fatigue” – article linked here, and “MTHFR” – article linked here) which people google and begin to self-diagnose and panic about.

What Is Th1 and Th2 Dominance?

To break down the science of the immune system in one blog article is not only not possible – it is part of the problem which gives people the wrong idea about our immune health.  It is not easy to simplify the functions and branches, roles and operations of our very complex immune systems.  When people try to (like bloggers on the internet) the result tends to be oversimplification.
However, I will try to explain what people mean when they conclude that they are Th1 or Th2 dominant.
They are referring to what are, loosely speaking, two different sorts of T cells produced by our adaptive immune system – the part of the immune system that learns and remembers threats and marshalls the ‘attack’ cells to the site of threats/invaders.
Th1 cells release cytokines (huge collections of chemicals, some of which can directly kill pathogens) which stimulate macrophages and dendritic cells (the cells that ‘eat’ or ‘kill’ pathogens) to an area where an invader or infection has been identified.
Th2 cells play a different role.  They activate B cells, which are lymphocytes responsible for the production and release of antibodies into blood and connective tissue to directly attack threats.  B cells also patrol the body for threats and memory B cells function to provide a more rapid response upon subsequent exposure to a previously seen pathogen.
Both of these types of T cells are known as ‘helper’ T cells, because they cannot directly kill invading pathogens but control the immune response by directing the cells which can to where they are needed.
It is theorised that part of autoimmunity is rooted in an imbalance of Th1 versus Th2 cells.  This kind of makes sense logically, in that too many Th2 cells will cause an overproduction of B cells and therefore a lot of antibodies and not enough cytokine activity.  Vice versa would also be true, causing a lot of cytokine production but very little antibody creation.
The problem is that we really, really don’t know enough about how the immune system works to make such a generalisation.
What we do know is that we have identified the following cells in the human body, thus far:

  • Th1
  • Th2
  • Th3
  • Th9
  • Th17
  • Th22
  • Tr1
  • Tfh

Whilst it may be true that the 3, 9, 17, 22 versions are less dominant than Th1 and Th2 – they complicate the picture of immunity.  Additionally, the role of T – r – 1 (written thus to make it clear that this is not T ’h’ 1!) cells is to control the activation of memory T cells and suppress Th1 and Th2 responses.

Autoimmunity – the Immune System Turned Inward

The whole issue with autoimmunity is the recognition of ‘self’ as a pathogen.  Whether that is one organ that is targeted, like the thyroid in both Hashimoto’s Thyroiditis and Graves’ Disease, or whether that is skin, as in eczema and lichen skin conditions or joint tissue as in Rheumatoid Arthritis, the theme is always the same.  At some point the immune system has recognised some form of ‘self’ protein as foreign and mounted an attack.
It must be recognised that this actually happens all the time, to everyone – not just those with a diagnosed autoimmune condition.  The reason the immune system is so complex and sprawling is because it contains within it not only the ‘activate’ portion to mount attacks, but also the ‘deactivate’ portion which stops an attack once the threat has been eliminated.
As such, there are whole pieces of our immune system which are designed to cannibalise the cells it produces – each T cell goes through a process of maturity in the thymus gland, during which it is tested both for the ability to interact with what is called the Major Histocompatibility Complex (MHC, see below) and also for binding to self-peptides (essentially protein fragments which are ‘us’ rather than proteins that are ‘enemies’).  B cells go through a similar testing for recognition of self, but this takes place in the bone marrow.
It is thought that 98% of T cells fail one of these tests.  

Major Histocompatibility Complex – an aside you can skip if you don’t need the science

The MHC is on the surface of macrophages or dendritic cells, which are basically inflammatory cells of the immune system.  These cells ‘eat’ pathogens, and then “present” them to the B cells and cytokines (essentially the army of troops which are going to be responsible for the major takedown and memory of what the macrophage or dendritic cell has found).  The way they do this is by showing a small fragment of the protein of the antigen they have ‘eaten’ to the adaptive immune system.  The ‘presentation’ is done in the MHC.  Think of the MHC like the label on an inflammatory cell – it shows the T cells and B cells and cytokines what’s inside, what they’re looking for in the body and to go forth and attack when they see that protein anywhere.


Autoimmunity – Where Does The Immune System Go Wrong?

It is thought that autoimmunity could potentially emerge out of several, different but linked issues:

Firstly, the natural process of suppression may break down and the regulatory T cells and Tr1 cells might not keep the killer cells in check.

Secondly, the thymus might not be doing a great job of preventing self antibodies from being released.  

Thirdly, those with autoimmune propensities tend also to have a high amount of inflammation which presents so much stress to the immune system that it may be overwhelmed and unable to differentiate accurately.

Lastly, those with autoimmune propensities tend to have a genetic predisposition which may also be accompanied by a genetic inability to make as many of the regulatory parts of the immune system.
Once a self-antibody has been created and allowed to survive, if it goes into an inflamed body and creates replicas etc. it is easy to see how a process of self-attack (i.e. autoimmunity) can persist and snowball.  

Autoimmunity is as much a flaw in what our immune system CAN’T DO (i.e. switch off) as what it can (i.e. attack ourselves)


Back To Th1, Th2

So we’ve currently moved quite far from the talk of Th1 or Th2 dominance… and that’s because the global picture of immunity is far, far, far bigger and more complex than boiling it down to the Th1 and Th2 cells.
That said, there have been links drawn from various autoimmune disorders back to the dominance of one or other of these immune cells.  However, whilst Hashimoto’s Thyroiditis is more frequently linked to Th1 dominance but it has also been shown to be linked to Th2 dominance.
What’s really important to focus on when it comes to addressing rogue immune function is less about the specifics of the immune cells that are overworking, underperforming and/or attacking the wrong things (i.e. self).  What really matters is the clinical utility of analysing the immune system in this way – which is where I get really infuriated when patients come to me from other practitioners who have been ‘treating’ them for their Th1 or Th2 dominance.
Some alternative professionals will ask their clients to spend large sums of money on supplements to ‘balance’ these supposedly warring factions of immunity.  Some foods and herbs are supposed to upregulate the immune side that you’re missing.  What these protocols fail to take into account is that the levels of Th1 and Th2 cells are SUPPOSED to fluctuate in the body.  Testing somebody by assessing how many of each is present in their blood is… shortsighted, to say the least.
Furthermore, the balancing protocols don’t take into account the presence of Th9, 17 and 22.  You literally cannot ‘balance’ someone’s immune function by targeting one arm of a poorly functioning immune system and thinking you’re effecting real change.  My theory is also that if the patient suddenly stops doing what they were doing to rectify their dominance their condition would immediately revert back to as they were before.
And lastly, immune systems are complex, as I’ve established.  There is no guarantee that using a herbal complex to stimulate the relevant part of the immune system will ONLY interact with that specific part, and some of the supplements I have seen have confusing ingredients which will either affect more than just the targeted part of the immune system OR are likely to do absolutely nothing at all.  Playing with this stuff isn’t sensible… and nor is it necessary.

So What Is Relevant With Autoimmunity?

There is no doubt that some misfiring and mistakes are happening with the T cells in autoimmunity.  There is a high probability that it is related to Th1 and Th2 dysregulation.  However, the relevant practices are more globally focused, rather than isolated to specifically tackle Th1 and Th2 cells.
The broader approaches are – as absolutely always – reduction of systemic inflammation, removal of external immune triggers such as toxins, moulds, chemicals and any foods that you are sensitive to, and introducing incredibly nourishing, nutrient dense foods into your diet to support your systems (ALL of your systems) from the inside out.
This really is the basis to all healthful pursuits – and has formed the foundation to every sensible treatment protocol forever.  This isn’t about shoring ourselves up or diagnosing ourselves with dominances and weaknesses and running around finding the adaptogenic herbs and modified chemicals that can apparently ‘balance’ us.  This is about healthy lifestyle practices – avoiding the things that activate immunity and stress our bodies whilst also taking time to take care of ourselves.

The best thing to ‘regulate’ T cell production, balancing Th1 and Th2 dominance, is to decrease inflammation.  Everything that you do to achieve this is the natural way of making the argument over whether you’re Th1 or Th2 dominant irrelevant.


  1. Robin P Clarke May 9, 2019 at 4:47 pm - Reply

    Right….. so how to reduce inflammation. Would be great if you put a link there!

    • victoriafenton May 10, 2019 at 1:21 am - Reply

      Hi Robin
      Thanks for the comment… though I’m not 100% what you mean? The sentence after ‘reducing inflammation’ was supposed to suggest ways in which you could do that. Inflammation is tricky though – what is one person’s lead domino for inflammation reduction isn’t someone else’s. In an article that was trying to campaign against super-granularity, I realise I’m running the risk of completely defeating my own argument – but reductions of inflammation, particularly where there is an autoimmune condition, will largely revolve around the largest sources of that inflammation for that person. But that annoying fact aside, you’re 100% right – we all waffle on about inflammation without specifically stating what it is and what to do about it. Will add this topic to my blog writing list and be sure to link out from here whenever it gets written! Thanks again for pointing out the required next steps in the discussion – always valuable and appreciated. Victoria

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