Jennifer Juno
@jenjuno.viralvaxlab.com
🇨🇦 in 🇦🇺 Scientist. Geek. Feminist. She/her. Lab head (viralvaxlab.com) at the Doherty Institute and University of Melbourne, interested in all things CD4/TFH/vaccine and virus-related. I stare at dots a lot.
8/9 In short, we suggest in vitro stimulation activates ag-specific T cells, which secrete cytokines and activate Treg and Th17/22 cells. Without careful phenotyping, all of these cells can get picked up as AIM+, accounting for the Th17-like memory cells found in many virus-specific AIM datasets.
December 20, 2024 at 3:39 AM
8/9 In short, we suggest in vitro stimulation activates ag-specific T cells, which secrete cytokines and activate Treg and Th17/22 cells. Without careful phenotyping, all of these cells can get picked up as AIM+, accounting for the Th17-like memory cells found in many virus-specific AIM datasets.
7/9 Mitch sorted tetramer-specific cells, labelled them, and added them back into PBMC before stimulating with the relevant peptide.
He was able to show that ag-specific CD4 cells downregulate CXCR4 while upregulating 4-1BB/CD137, giving us a more accurate way to define antigen specificity.
He was able to show that ag-specific CD4 cells downregulate CXCR4 while upregulating 4-1BB/CD137, giving us a more accurate way to define antigen specificity.
December 20, 2024 at 3:39 AM
7/9 Mitch sorted tetramer-specific cells, labelled them, and added them back into PBMC before stimulating with the relevant peptide.
He was able to show that ag-specific CD4 cells downregulate CXCR4 while upregulating 4-1BB/CD137, giving us a more accurate way to define antigen specificity.
He was able to show that ag-specific CD4 cells downregulate CXCR4 while upregulating 4-1BB/CD137, giving us a more accurate way to define antigen specificity.
5/9 Using RNAseq and confirmatory FACS, Mitch showed that CD39+ Tregs and Th17/Th22 cells expressing CCR6 and high levels of CD26 were being activated through the transwell via a mechanism involving IL-2.
These same subsets are also found during standard peptide-based AIM assays.
These same subsets are also found during standard peptide-based AIM assays.
December 20, 2024 at 3:39 AM
5/9 Using RNAseq and confirmatory FACS, Mitch showed that CD39+ Tregs and Th17/Th22 cells expressing CCR6 and high levels of CD26 were being activated through the transwell via a mechanism involving IL-2.
These same subsets are also found during standard peptide-based AIM assays.
These same subsets are also found during standard peptide-based AIM assays.
4/9 Possibly!
In a transwell assay, anti-CD3/CD28 stimulation can drive T cells in an adjacent chamber to express common activation markers (CD25, OX-40, 4-1BB, CD40L).
All of these responding cells had a memory phenotype, and were strongly enriched for CCR6 expression.
In a transwell assay, anti-CD3/CD28 stimulation can drive T cells in an adjacent chamber to express common activation markers (CD25, OX-40, 4-1BB, CD40L).
All of these responding cells had a memory phenotype, and were strongly enriched for CCR6 expression.
December 20, 2024 at 3:39 AM
4/9 Possibly!
In a transwell assay, anti-CD3/CD28 stimulation can drive T cells in an adjacent chamber to express common activation markers (CD25, OX-40, 4-1BB, CD40L).
All of these responding cells had a memory phenotype, and were strongly enriched for CCR6 expression.
In a transwell assay, anti-CD3/CD28 stimulation can drive T cells in an adjacent chamber to express common activation markers (CD25, OX-40, 4-1BB, CD40L).
All of these responding cells had a memory phenotype, and were strongly enriched for CCR6 expression.
2/9 Recently, though, we’ve been bothered by something we couldn’t explain: we find a lot of Th17-like, CCR6+ SARS-CoV-2 spike-specific CD4 T cells in our AIM assays, but we never see these cells when we use spike-specific class II tetramers.
Why?
Why?
December 20, 2024 at 3:39 AM
2/9 Recently, though, we’ve been bothered by something we couldn’t explain: we find a lot of Th17-like, CCR6+ SARS-CoV-2 spike-specific CD4 T cells in our AIM assays, but we never see these cells when we use spike-specific class II tetramers.
Why?
Why?