Read on Twitter
1/n
There are many things about my paper that just came out today in mBio that I would like to share with you all, both about the science, and about the people behind the science. If you're up for a thread, then here is your behind the scenes tweetorial: https://mbio.asm.org/content/11/3/e01293-20
There are many things about my paper that just came out today in mBio that I would like to share with you all, both about the science, and about the people behind the science. If you're up for a thread, then here is your behind the scenes tweetorial: https://mbio.asm.org/content/11/3/e01293-20
2/n
CD47 is a protein which signals "don't eat me" to your immune system which is constantly surveying for aberrant or foreign things to clear from the body. CD47 expression on the outside of a cell is one of the ways your cells signal that all is well but this can backfire.
CD47 is a protein which signals "don't eat me" to your immune system which is constantly surveying for aberrant or foreign things to clear from the body. CD47 expression on the outside of a cell is one of the ways your cells signal that all is well but this can backfire.
3/n
SO many people were involved in this study, and even more have been helping us with other aspects of our investigations into CD47 dependent regulation of immune responses. If you think immunologists just say CDblah blah blah, I will try to break it down as we go along.
SO many people were involved in this study, and even more have been helping us with other aspects of our investigations into CD47 dependent regulation of immune responses. If you think immunologists just say CDblah blah blah, I will try to break it down as we go along.
4/n
Those on Twitter are @StemCellBear @mayer_barber @PhoebeYiu1 @CesarLopezAngel @PaigeSHansen @Sarah00Galloway @monack_lab and so many more not on Twitter - all in all 35 authors from 14 institutions. "Why so many?" you ask. Did this paper "need" SO many authors? Let's see.
Those on Twitter are @StemCellBear @mayer_barber @PhoebeYiu1 @CesarLopezAngel @PaigeSHansen @Sarah00Galloway @monack_lab and so many more not on Twitter - all in all 35 authors from 14 institutions. "Why so many?" you ask. Did this paper "need" SO many authors? Let's see.
5/n
In this paper we examined 8 different infections, both viral and bacterial, and how they impacted CD47 expression (the "don't eat me" signal) on infected cells. We found that cells increase expression of CD47 as a default response to recognition of infection.
In this paper we examined 8 different infections, both viral and bacterial, and how they impacted CD47 expression (the "don't eat me" signal) on infected cells. We found that cells increase expression of CD47 as a default response to recognition of infection.
6/n
At the last possible moment between the 1st and 2nd response to reviewers we added in an analysis of @virusninja's SARS-CoV-2 infected cells data and saw that CD47 was upregulated there as well. Since submission we have found this in many other data sets of SARS-CoV-2.
At the last possible moment between the 1st and 2nd response to reviewers we added in an analysis of @virusninja's SARS-CoV-2 infected cells data and saw that CD47 was upregulated there as well. Since submission we have found this in many other data sets of SARS-CoV-2.
7/n
Specifically, in regards to that last piece of data which is not published anywhere, CD47 shows a 0.88 log fold change from none to high SARS-CoV-2 viral load with a Q value of 3.15e-10. Easy to look up any gene you're interested in https://twitter.com/mason_lab/status/1263838646593093632?s=20
Specifically, in regards to that last piece of data which is not published anywhere, CD47 shows a 0.88 log fold change from none to high SARS-CoV-2 viral load with a Q value of 3.15e-10. Easy to look up any gene you're interested in https://twitter.com/mason_lab/status/1263838646593093632?s=20
8/n
As we see from so many other infections, the increase in CD47 is low fold change but statistically significant. We find this consistently across viruses, bacteria, parasites, and even if we trick cells into thinking there is an infection when there is not, as with R848 stim.
As we see from so many other infections, the increase in CD47 is low fold change but statistically significant. We find this consistently across viruses, bacteria, parasites, and even if we trick cells into thinking there is an infection when there is not, as with R848 stim.
9/n
For all of the different infections we wanted to investigate, we collaborated with groups that had those infection models in their labs, and were willing to enter into this exploration with us of how infections impact CD47.
For all of the different infections we wanted to investigate, we collaborated with groups that had those infection models in their labs, and were willing to enter into this exploration with us of how infections impact CD47.
10/n
with @CesarLopezAngel, Ed Pham, Mark Davis, Aijaz Ahmed, and Jeff Glenn we were able to look at CD47 in the sofosbuvir trial at Stanford in 2013. Yes, we've been working on this paper for a very long time. We saw that the inflammatory mileu triggered by HCV upregulates CD47.
with @CesarLopezAngel, Ed Pham, Mark Davis, Aijaz Ahmed, and Jeff Glenn we were able to look at CD47 in the sofosbuvir trial at Stanford in 2013. Yes, we've been working on this paper for a very long time. We saw that the inflammatory mileu triggered by HCV upregulates CD47.
To be continued...
