My problem is that there seems to be evidence that supports both sides interpretations. If it was just a question of being ´in a position to assess it,´ then surely all the immunologists would agree with you?
What evidence runs contrary to what I am suggesting? I totally agree that B cells produce cytokines but they do so in environments where 'inflammation' does not apply. Most immunologists are not in a position to understand this, it seems. Whether it is because they are not very good at putting together complex dynamic ideas or whether they have just had no training in tissue microanatomy I have never really understood but I suspect it is the former. Immunodynamics are so complicated that most people simply cannot get their heads around it. Honest people like my wife, who is highly intelligent and a medical expert in another field, just say they cannot handle it. The problem is that people who have become immunologists who are not able to get their heads around the complexity latch on to simple catchy ideas in review articles without worrying about the fct that they do not add up.
Perhaps a practical point would help. Cytokines are signals from one cell to another. In general they operate in microenvironments - so the concentration generated in a cell cluster of volume 1 nanolitre may be millions or even billions of times higher than the concentration resulting when the cytokine diffuses out into blood and ECF. So cytokines in blood in general do not cause inflammation.
What is inflammation? It is an increase in permeability to fluid of blood vessels and an exit of white cells into the tissue. What would that be in spleen, where B cell produce cytokines? The problem is that splenic vessels are totally permeable anyway and the white pulp tissue is totally made up of white cells anyway. So you cannot really have inflammation of the spleen. The spleen is a bag of inflammation to start with in a sense.
The other key point is that cytokine production by B cells is mostly just a step in the co-operative process that leads to antibody production. So blocking B cell cytokines is just blocking antibody production and if you take away all the B cells it does not matter which step you think you are blocking because all the steps have gone. It would be different if B cells stimulated T cells to go off and cause inflammation in autoimmunity on their own. The problem with this is that nobody has ever found any self-reactive t cells that might do this in autoimmunity. Virtually all immunologists believe in autoreactive T cells despite none ever having been found, just as people believe in gods and free will despite them never having been found. But to take autoreactive T cells seriously we need some empirical evidence for their existence.
At root I guess the problem may be that not that many people in academic disciplines are actually any good at assessing what theory is truly supported by evidence. That may seem surprising but the 2008 crash showed it to the case for 95% of economists and there does not seem to be a single psychiatrist in the UK capable of seeing that the evidence for using CBT in ME is zero. And then there is Donal Trump running for president. Human discernment does seem to be a bit unreliable in a range of fields! By and large people go on believing what they want to believe.