Todays paper I read from Science Immunology 2026 creates a new mechanism for CD20-depleting antibodies. Immunologists have suggested that CD20-depleting antibodies work because they are affecting T cells. One idea is because T cells are suggested to nibble B cells to take CD20 onto their surface and they are killed. I don’t buy this because many of the CD20 T cells are naive suggesting they havent had antigen presentation by B cells and importantly CD19 antibodies work and very few, if any, T cells have CD19 on their surface so the mechanism much be different.
Some T cells, notably CD8 T cells can make CD20 and they do get depleted but the people suggesting these ideas have spent alot of time convincing us that it is not CD8 that is really important but TH17 CD4 T cells.
Now I have suggested…Why make such complicated explanations to explain how CD20-depleting antibodies work. Isn’t the simplist idea because they deplete CD20-B cells becuase B cells can do many of the things that can drive inflammation, the easy one would because they produce proteins that activate white blood and other cells. Another one is it gets rid of EBV
Then we have the T cell immunologists view that B cells are depleted and so they cannot present the pathogenic target molecule and so do not activate T cells.
Now I would have thought tumour necrosis factor alpha or beta could be things that B cells produce that could be important. However this recent paper in mice its suggest that it is interleukin 17 produced (IL-17) by B cells that are important for disease. So a new mechanism. Does this B cell IL-17 work because it acts on T cells or is it working on B cells? B cells express IL-17 receptors so they respond to IL17 such as IL-17A and IL-17F. Apparently, this enables them to promote B-cell proliferation, differentiation and antibody production.
Now I have to say OK… a new possibility, but I must admit I do not buy this. First thing is that based on our and other people’s work CD20-depleting to nothing or very little to mice, so who cares what B cell antibodies do to mice. Next there have been lots of other studies questioning whether IL-17 deficiency is essential in mice and importantly in multiple sclerosis. Now the central question in the paper is
“Is an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease?” According to this study they get the answer from the “Man from Delmonte (Paragraph 2)” but I wonder if it is science from Dellboy.
AI..Where is the intelligence going to come from? Who needs Intelligence when you say B cells
Now to address the above question I go to Artificial Intelligence. It seems these days that AI is putting humans out to grass and not a moment too soon for me… I hear you say 
Give the students a project and it is straight on to AI to give the answer and the write-up…….Students have become customers these days and they want their degrees and feedback and marking done quickly….So it seems universities are going to turn this full circle and use AI to do the marking…What a mess. Let’s cut out the middleman and forget about education and thought. Pay the money and they get Robotic degrees:-(
I guess that AI will be the direction of travel for the review of papers and maybe if they had used AI this paper may have not seen the light of day. I asked Chat GTP and what does it say to the above question
Chat GTP says
No—an adaptive cellular source of IL-17 is not absolutely required for the induction of Experimental Autoimmune Encephalomyelitis (EAE).
But the paper says “Here, we….demonstrate that an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease.”
Now first thing first I have to accept that AI makes stuff up when it doesn’t know the answer. But my reading would give counter arguments but the great and the good can be persuasive:-(
COI None
Disclaimer my views
Source: multiple-sclerosis-research.org