delcake

fear, 11 months ago

Reddit isn't going to die overnight. It will probably not die at all (at least not as a result of this latest stupidity). And that shouldn't be anyone's goal here, anyways. The goal should be to fracture the monopoly. Let the dregs stay on Reddit. And that's not me calling every redditor at the moment a dreg. I mean allow it to devolve into that, just like how Twitter is devolving into nothing but twits.

Trust me, reddit remaining alive is good for the fediverse. Let it become an echo chamber that helps contain the kind of person no one needs over here. This is going to be a slow process. The fact that this site is already functional is a really good sign that the process is going to work. Don't rush it, just sit back and let it happen.

AdmiralSnackbar, 11 months ago

The article actually does a decent job of summing up the idea, but I always like to read the abstracts themselves, so here's that for anyone that's interested.

Abstract

In solid tumours, the abundance of macrophages is typically associated with a poor prognosis. However, macrophage clusters in tumour-cell nests have been associated with survival in some tumour types. Here, by using tumour organoids comprising macrophages and cancer cells opsonized via a monoclonal antibody, we show that highly ordered clusters of macrophages cooperatively phagocytose cancer cells to suppress tumour growth. In mice with poorly immunogenic tumours, the systemic delivery of macrophages with signal-regulatory protein alpha (SIRPα) genetically knocked out or else with blockade of the CD47–SIRPα macrophage checkpoint was combined with the monoclonal antibody and subsequently triggered the production of endogenous tumour-opsonizing immunoglobulin G, substantially increased the survival of the animals and helped confer durable protection from tumour re-challenge and metastasis. Maximizing phagocytic potency by increasing macrophage numbers, by tumour-cell opsonization and by disrupting the phagocytic checkpoint CD47–SIRPα may lead to durable anti-tumour responses in solid cancers.

In English:

When you have cancer, a large amount of white blood cells (WBCs) is usually a bad sign. Sometimes it's not though. In this paper, we made mock tumors with WBCs and cancer cells. We used antibodies to mark them for destruction by WBCs and found that it actually worked, that is, the WBCs worked together to stop the tumor from growing further (this is important because many times cancer will mutate to avoid detection from the immune system). We then took some mice with cancer and did two things to them: 1.) We gave them white blood cells with genetic modifications that cause the WBCs to ignore the signal from the tumor that says "don't eat me!" and 2.) We gave them some monoclonal antibodies. Doing these two things caused the bodies of the mice to spontaneously start marking the tumor for destruction by WBCs. This resulted in increased survival rates for the mice, and decreased the likelihood that the cancer would worsen in the future.

If I made any mistakes, please let me know. My degree is not in biology but I did take advanced cell biology classes as part of it.

Some other links:

DOI: https://doi.org/10.1038/s41551-023-01031-3

More on the CD47-SIRPα immune checkpoint: cell.com