We are entering a new, endemic stage of #COVID19 spread. Drop in efficacy (50% or less) against new SA variants is a classical example of vaccine efficacy against #influenza virus.
It is clear from all available data that both @BioNTech_Group and @moderna_tx mRNA vaccines will be less effective against SA variant and there will be many more like this.
@BioNTech_Group @moderna_tx but we will have a bigger problem than SA variant of #SARS_CoV_2. And it has to do with the little-understood phenomenon of "original antigenic sin" [OAS]. The idea that @moderna_tx or @BioNTech_Group will simply design new #mRNA #vaccines against SA variant, will not work here.
@BioNTech_Group @moderna_tx Anybody already vaccinated with the original #mRNA or #Vector #vaccine or recovered from the original #SARS_CoV_2 will have antibodies that will prevent booster uptake and priming against new antigenic epitopes. This is a reason why #influenza vaccines are minimally effective.
@BioNTech_Group @moderna_tx there is no way around it.If @moderna_tx or @BioNTech_Group will try to design an mRNA vaccine that bypasses original Ab epitopes and only includes new epitopes, it could lead to memory T cell only,dominant response, and worse outcome as T cells only response is very detrimental.
@BioNTech_Group @moderna_tx the best solution is to design new mRNA or Vector vaccines that already includes both new and old epitopes. But there always will be new variants, over and over again, that will escape all previous iterations. It is new, 21st-century #influenza behavior.

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More from @3DiMMUNE

19 Jan
In this opinion paper @RMedzhitov went back to drawing board to update his views on #allergy and how it could develop.

#immunology

I read this paper and here is my take on it

1/
@RMedzhitov Why focus on allergy? b/c allergy is a paradox. The allergy we recognize is a completely maladaptive response and has no protective role whatsoever. It is not clear why do we even need IgE

2/
@RMedzhitov So, some 10 years ago or so, @RMedzhitov started to suggest that #allergy is an intrinsic property of a certain type of #antigens, many of them with enzymatic function (enzymes). 3/
Read 24 tweets
19 Apr 20
let's talk about #CytokineStorm in #COVID19.

1st, there is no standard threshold above which something is called #CytokineStorm.

Mechanistically, the simplest form of #CytokineStorm we can understand is when anti-CD19 #CART cells are infused in tumor-bearing recipients.
in this scenario, we have large numbers of antigen-specific T cells (anti-CD19) and large numbers of antigen-bearing cells (CD19+ tumor cells). When too many T cells engage with too many antigens simultaneously in a short period of time we get #CytokineStorm
Why is that? This is because naturally developing an adaptive immune system (T cells) ordinarily doesn't work that way. 1st, for a given antigen we have very few antigen-specific T cells (~ 50 cells/antigen, unlike anti-CD19 CAR-T cells that are in millions).
Read 16 tweets
15 Apr 20
a removal of a subset of #Tregs called T follicular regulatory cells (Tfr) from the immune system in #Foxp3-cre Bcl6-fl/fl mice #paradoxically reduces, rather than increases, #peanut-specific #IgE responses.

#immunology

bit.ly/2RAMe8L
And if you think maybe their knockout mice are some kind of weirdos, not really. Their model also shows that total IgE is increasing as expected. So, the system the authors are using is within acceptable norms.

bit.ly/2RAMe8L
The authors then went on to show that IL-10 derived from Tfr cells are important for promoting peanut allergy-producing IgE production. (IL-10 is lesser understood cytokine but it is generally accepted as an immunosuppressant.) #immunology
Read 14 tweets
7 Apr 20
#Antibody response usually protects against infection/re-infection but #Tcells could protect against clinical signs of disease. #COVID19
The paper from #1990 analyzed the antibody response and clinical symptoms of the common cold #coronavirus #229E. Neutralizing antibody titers declined within 1 year after 1st challenge, and 70% from the "immunized" cohort got re-infected but none showed clinical symptoms.
This most likely explanation is that clinical symptoms were controlled by virus-specific T cells. There is an assumption here that a protective level of antibody would have prevented re-infection in the first plays
Read 11 tweets
10 Jan 19
A new paper in @sciencemagazine from #Belkaid lab at #NIH described an #alternative differentiation #pathway for #commensal-specific T cells in presence of inflammation. Do the data presented support conclusions? Let's dive in.

science.sciencemag.org/content/363/64…
1. #Commnesal S. epidermidis–specific -#MIIINA:H2-M3+ CD8+ T cells ordinarily differentiate into Tc1 or Tc17 subsets. However, when co-exposed to chitin or sand fly (source of #inflammation), Tc17 subset also produce type II cytokines.
2. In such condition, type II #cytokines such as IL-5 or IL-13 are produced by CCR6+ Tc17 cells (out of which 30% are IL-17+). However, there is no overlap between IL-17+ and IL-5+/IL-13+ CD8+ T cells. So, the authors conclusion about "paradoxical phenotype" is unsubstantiated.
Read 10 tweets

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