Interleukin-6 (IL-6) and IL-6 autoantibodies

Interleukin-6 (IL-6) is a cytokine, i.e. a messenger used by cells of the immune system and many other tissues to communicate. It is produced by scavenger cells, lymphocytes, connective tissue cells, vessel walls and, during physical work, also by the muscles. The test catalogue does not determine IL-6 itself but autoantibodies against IL-6 – in serum, as part of the autoantibody screens for long/post-COVID and chronic fatigue syndrome. Such antibodies can weaken the effect of the body's own messenger. To interpret them, it helps to understand what IL-6 normally triggers in the body.

What IL-6 does in the body

IL-6 acts via a receptor that, together with the signalling protein gp130, passes the message into the cell interior. In the liver, IL-6 stimulates the formation of the acute-phase proteins, including CRP, fibrinogen and hepcidin – the latter holds iron back in the stores and withholds it from pathogens. In the brain, IL-6 triggers fever via prostaglandins and influences sleep, appetite and drive. It helps B cells mature into antibody-producing plasma cells and steers the development of certain T cells. It also activates the stress axis with release of cortisol. Released from the muscles, IL-6 additionally acts on sugar and fat metabolism.

High IL-6 – what happens in the body?

With infections, injuries and inflammation, IL-6 rises within hours. The liver then makes more CRP, body temperature rises, and the typical feeling of illness develops, with tiredness, loss of appetite and withdrawal. If IL-6 remains raised for a long time, for example in chronic inflammatory diseases, iron is held back permanently, which can lead to anaemia of inflammation; muscle loss and changes in sugar metabolism are also favoured. Studies have observed raised IL-6 levels in persistent symptoms after COVID-19 and in states of exhaustion, but the findings are inconsistent. Very high levels occur in severe courses with an excessive immune reaction.

Autoantibodies against IL-6 – what happens in the body?

Autoantibodies against IL-6 bind to the messenger and can neutralise it, so that it reaches its receptor less well. The response to infections is then weaker: the liver makes less CRP and fever stays lower, even though inflammation is under way. Individual case reports have described strongly neutralising IL-6 autoantibodies in people with recurrent bacterial skin and soft-tissue infections. After SARS-CoV-2 infections, studies have observed more autoantibodies against various messengers and receptors; what role they play in long/post-COVID and in chronic fatigue syndrome is still being researched and is disputed. Low or absent autoantibodies are the normal case.

The interpretation is given in your report.