ApuXan® stimulates the immune system in a controlled manner

How the immune system fights viral infections

How the immune system fights viral infections such as the corona virus (SARS-CoV-2)?

The immune system is the body’s own protective system for the defence against foreign or toxic substances or pathogens such as viruses.

Our immune system can fight viruses in two ways:

  • antibody production
  • T-killer cells (cytotoxic T cells)


Figure 1: Only certain specific antibodies fit to a pathogen (e.g. virus), just as only a certain key fits to a lock


Formation of neutralizing antibodies:

To defend against pathogens (e.g. viruses or bacteria), defence cells in our body produce tailor-made antibodies called neutralising antibodies. These circulate in the blood and can quickly recognise, bind and kill pathogens. It takes about five days from the beginning of the virus infection until a sufficient number of suitable antibodies are available.

However, the antibodies only recognize a specific virus. Only this one virus fits exactly like a key into the antibody lock (Figure 1). If the virus (mutation) changes, e.g. during a flu epidemic or in the following year, new antibodies must be produced by the organism. This means that we have to survive a viral infection each time before antibodies are formed that protect us from the same virus during the next infection. If the virus changes, we have no protection against the next infection.

Defence by T-killer cells (cytotoxic cells):

The second important way to fight viruses is through T-killer cells. They are also called cytotoxic T cells (from “cyto”, ancient Greek: cell and “toxikon”, ancient Greek: poison). After a viral infection, T-killer cells are produced in sufficient quantities by our organism with a delay of several days.

According to Prof. Drosten (head of the Institute of Virology at the Charité Berlin), T-killer cells are the actual reason why viral diseases such as “corona disease” are stopped. They recognise body cells affected by the virus and immediately cause their destruction and removal from the body. This also makes these viruses harmless, which are already in the body cell (see figure 2).


Figure 2: Destruction of virus-infected body cells by T-killer cells


However, the formation of T-killer cells occurs only after days of infection with e.g. SARS-CoV-2 (corona virus) and can often be too late for people who belong to the risk group. A similar example is the SARS pandemic that spread from southern China in 2002/2003. SARS is also transmitted by corona viruses and causes severe acute respiratory syndrome. In the SARS pandemic, 80-90% of infected patients were found to have a sharp drop in T-killer cells compared to the healthy control group [3]. Thus, SARS has reduced the T-killer cells to such an extent that the body’s own immune response is weak.

This is the reason why patients with a weakened immune system belong to the risk group and are particularly at risk for severe disease progression. This includes patients who suffer from diseases that are associated with an immune deficiency, e.g. chronic inflammatory bowel diseases, tumour diseases or by taking medication that weakens the immune defence, e.g. cortisone. Elderly people and patients with other pre-existing conditions, e.g. diabetes mellitus, asthma, are also particularly at risk.

The delayed immune response by means of T-killer cells is thus the cause of the delayed destruction of the virus and can thus lead to death in the worst case. It is therefore necessary to prepare the immune system for an infection – to train it in a controlled way.

How does ApuXan® stimulate the immune system in a controlled way?

The spray ApuXan® is applied into the oral mucosa and under the tongue. Special immune cells (Langerhans cells, a subtype of dendritic cells) patrol the oral mucosa. The Langerhans cells recognize the active substance beta 1-3/1-6 -glucan of ApuXan as a quasi-pathogenic (foreign substance) via special receptors and trigger the controlled stimulation of cytotoxic T cells via an immune cascade.

These T-killer cells then migrate to the site of infection, e.g. the throat or lungs. I.e. beta 1-3/1-6 glucan trains the immune system and prepares it unspecifically for an upcoming infection. When the infection occurs, the immune system is already prepared and can react immediately via the T-killer cells and neutralize viruses of any kind.

Why is ApuXan® more effective than other beta-glucan or medicinal mushroom products?

In medicinal mushrooms, beta-glucans are components of the cell wall and thus often integrated into a scaffold of other cell wall components. This can impede immunological recognition by dendritic cells, Langerhans cells or lymphocytes via their respective receptors. Although extracts have a higher beta-glucan concentration, they are still poorly soluble in water and thus difficult to absorb by the body.

Decisive for the recognition of beta 1-3/1-6 glucan by the receptors of the immune cells is that beta 1-3/1-6 glucan is freely available and thus no longer bound into the cell walls of the medicinal mushrooms. The PuranoTec® manufacturing process of ApuXan® quasi exposes beta 1-3/1-6 glucan by a very strong comminution down to below 0.4 µm and thus makes it very easily detectable for immune cells, which leads to an effective immune cascade. Due to the small particle size of beta 1-3/1-6-glucan in ApuXan®, beta 1-3/1-6-glucan can not only be detected but also phagocitated (eaten) by immune cells, which is a prerequisite for immune stimulation.

For macrophages it could be shown that particles with a size of 0.5 µm are absorbed 80% better than those with a size of 4.5 µm [1]. From a size of 15 to 25 µm, the macrophages reach their limits and can no longer absorb these particles. For particles larger than 10 µm, an immune response via macrophages is thus almost impossible. Medical fungi or beta-glucan products in capsule form are considerably larger than 10 µm with an average particle size of over 100 µm.


[1] Pacheco, P., White, D. & Sulchek, T. Effects of microparticle size and Fc density on macrophage phagocytosis. PLoS One 8, e60989, doi:10.1371/journal.pone.0060989 (2013).