> Through a series of experiments, the researchers found that T cells could indeed self-activate by puckering their cell membrane inwards to allow the B7 protein and the CD28 receptor to bind to each other
Very cool, but doesn't this imply that T-cells can also activate other T-cells that are nearby? (in trans)
Edit: in the actual paper they said "We generated reporter Jurkat lines and Raji APCs stably expressing CD80, CD86, or neither (Figure S2A), enabling coculture conditions in which the B7 ligand was presented to CD28 in cis, in trans, or both. To minimize potential trans-B7:CD28 interactions between T cells, we cultured Jurkat reporter cells with 100-fold excess of Raji APCs"
However, the point remains that in vivo, T-cells would be able to do both the cis and trans activation. Which is still novel, I think?
I'm pretty sure I've heard that they can, I have no source for this though. I wonder if this is linked to phenomena such as spontaneous degranulation in the complete absence of an antigen in mast cell disorders (once again, not positive this is a thing, but I believe it is).
Though on that last point IIRC, I believe I've heard it also just has to do a bit with random conformational noise on the receptors causing autoactivation.
Wasn't this already known, or at least suspected? I thought the bigger unknown was how to activate the T-cells, since tumor cells are very good at masking like normal tissue. The article lightly touches on that (when talking about the process of T-cell self-activation), but it still doesn't specify on how to control that targeting.
So I'm not sure how the research matches the headline. What's the link that I'm missing? Yes, T-cells can activate themselves, which has implications both for tumors and for auto-immune diseases (which was the first thought that came to me while reading), but this research does not actually bring us closer to weaponizing them?
but when this happens in real life, it looks like mass shootings
i.e., I'm saying (due to how I think) that in the layer of the cells, like the biological cells that come together to form one human, a T cell activates itself to fight tumors (damaged tissues? organism mistakes?)...
is somehow comparable to a human person snaps, "goes postal", or things like this. (keep in mind that some places are truly deep within the 'cancer tissue'; and yea, this whole comment implies viewpoint that 'civilization is cancer' or something like that)
I've seen some movies that could be like this too, like "sleeper agent gets activated" trope, or other kinds of anamnesis-processes making people suddenly act far from the norms
There is nothing in the behavior of cells that is reflective of human intelligence.
Cells are "amino acid robots."
They string the 26 programmed amino acids into exotic plastics/proteins to execute their programmed functions.
There is no relation to human behavior in cellular behavior.
At the end of an infection, most immune cells trigger "apoptosis" (controlled cellular "suicide").
At the end of a riot, police obviously do not do this.
You might find this Kurzgesagt introduction to immune system behavior interesting. There are several videos in this sequence, and Kurzgesagt ultimately published a book that is worth reading.
This skips around, and misses major aspects that are barely mentioned.
The compliment system has it's own video in the Kurzgesagt series, although it misses a major aspect in a "membrane attack complex" in the participation of an antibody.
This first entry in the series that you've posted focuses on the innate immune system, but barely mentions compliment, and doesn't mention C-3 or a membrane attack complex. Dendritic cells are also left out, but they may be in another episode.
I'll watch the rest of the series, but I think that Kurzgesagt has more focus.
Very cool, but doesn't this imply that T-cells can also activate other T-cells that are nearby? (in trans)
Edit: in the actual paper they said "We generated reporter Jurkat lines and Raji APCs stably expressing CD80, CD86, or neither (Figure S2A), enabling coculture conditions in which the B7 ligand was presented to CD28 in cis, in trans, or both. To minimize potential trans-B7:CD28 interactions between T cells, we cultured Jurkat reporter cells with 100-fold excess of Raji APCs"
However, the point remains that in vivo, T-cells would be able to do both the cis and trans activation. Which is still novel, I think?