I would forget the idea of 'inflammatory marker'. This is an idea thought up by clinicians who do not understand immunology - or inflammation. Your three cytokines each have several different roles and will tell you something different in each of many different contexts. Inflammatory markers are like the ingredients in cooking. An egg goes well in a cake and an omelette. Onions go well in an omelette but not in a cake. Butter is good on french beans but not on cauliflower, which is better with cheese. Rheumatoid arthritis uses TNF but skin conditions may use IL-1. Interleukin-6 blockade is good in RA but not in psoriatic arthritis. Interleukin-1 RA is fantastic in rare hereditary autoinflammatory syndromes but not much good in RA. The interest is in the differences between each process. Inflammation is an old fashioned term, like cooking, that may be useful in a book title but not much inside! 

Alright, thanks.

But somehow I / we have to integrate those items into our study. So as far as I understood there is a main difference for the 3 different interleukines which means I have to describe them seperately. I am surprised that the term "inflammatory marker" is a old fashioned term because I read this in different studies (which are from 2010,2011,....) However, time is moving fast. Thanks for the answer and the explanation

Dear Erich,

Maybe the problem is that time is moving rather slowly! I think 'inflammatory marker' was invented around 1980 as a term for something to measure in drug studies of conditions like rheumatoid arthritis that indicated a more fundamental effect on disease mechanisms than could be achieved with 'anti-inflammatories' like ibuprofen. It is, of course,  ironic that 'inflammatory markers' are not affected by 'anti-inflammatories', which do reduce acute inflammatory features like pain and oedema. But in 1980, as a generic term for high ESR, CRP and low Hb etc. the term may have had some value. It became fashionable for rheumatologists and other physicians to glibly talk of inflammatory markers, when they had no idea quite what they meant.

Science is dominated by fashion and fashion tends to lag fifteen to twenty years (maybe thirty five in this case) behind cutting edge thinking. That is why there are still lots of studies talking about inflammatory markers. But in RA we are now in an era where drugs target specific cell types or cytokines. There is a need to have a more specific terminology - although I am not sure that many clinicians have really much more idea than they ever did. So if a patient is given tocilizumab to block IL-6 there is no point in using CRP as a measure of effect on inflammation because the drug blocks the production of CRP directly, whether or not there is any change in inflammation. So the CRP is no longer in all situations an inflammatory marker. The ESR is too non-specific to be bothered with now. IL-10 switches T cells from talking to macrophages to talking to B cells. That is important in the genesis of certain types of inflammation but probably has the opposite effect in others. 

To be honest, if you are reading papers that talk about inflammatory markers in 2011 they are probably not the sort of papers you really want to be reading. Maybe you need to start somewhere but you want to avoid becoming part of the fashion that turns the same old handle for forty years.