Pieter Meysman

Challenges and Future Directions of AIRR-seq-Based Diagnostics Adaptive Immune Receptor Repertoire sequencing (AIRR-seq) is a promising diagnostic method across various clinical conditions, yet its widespread impl…

The AIRR Diagnostics WG commentary is now available, wherein our members discuss both the challenges of current #AIRR-based #diagnostics, as well as the future directions that we see the field going into!
www.sciencedirect.com/science/arti...

That's it. #ATCR25 is over!
Thanks again to all attendees, speakers and support staff for making this an amazing meeting!

Last #ATCR25 speaker: Paul Thomas on deciphering the T cell receptor recognition code.

Fifth speaker on #ATCR25 day 2: Michael Birnbaum on high throughput TCR analysis and generation.

Fifth speaker, #ATCR25 day 2: Encarnita Mariotti-Ferrandiz on TCR repertoire signatures in auto immune and infectious disease.

Fourth speaker, #ATCR25 day 2: Hashem Koohy on decoding antigen-specific T cell recognition.

Third speaker, #ATCR25 day 2, Soumya Raychaudhuri on how the HLA affects the TCR repertoire, and how the TCR affects cell fate.

MHC peptide predictions are accurate but fail to identify the few immunodominant epitopes within the larger list of binders.

There many epitopes that could induce a strong T cell response, but do not get processed from their protein and do not get presented.

Second speaker, #ATCR25 day 2: Antonio Lanzavecchia on CD8 T cell immunodominance

Immunogenecity might not be the best sole criteria for the basis of vaccines, epitopes need to be protective too. This is hard but doable to figure out.

Organoids might be a way forward, but not the answer to everything (but could be the answer to a lot of things)

The spleen harbor a collection of different immune cells, and contain memory of infection and vaccination.

Next topic: two classes of regulatory T cells: CD4 Foxp3 T cells regulating B cells and a CD8 regulatory subset using granzyme B regulating T cell auto reactivity.

Exposure to pathogens (Mtb, CMV,...) remodels our immune system in a way that benefits them (and may hurt us)

Within TCR repertoires are motif clusters linked to disease progression, suggesting the existence of 'distractopes', epitopes that the disease wants you to react to, as a 'smoke screen' to redirect or exhaust the immune system.

Investigating the way that Mtb evades the immune system lead to the innovation of looking at the TCRs from tetramer sorting experiments.

Second topic: failures in vaccine trials. An infectious disease only becomes 'famous' when it learns how to evade our immune system.

First topic: how do human immune systems compare to inbred mice? Mice are the 'starter car', simple but lacking complexity, leading to failure in mice models.

First speaker, second #ATCR25 day: Mark Davis on analyzing the T cell response.

#ATCR25 short talk 8: Nicole Mifsud on the immune signatures of alloreactive T cells during transplantation rejection.

#ATCR25 short talk 7: Vincent Van Deuren on using TRIASSIC to identify convergent TCR clusters in the synovial fluid of rheumatoid arthritis patients.

#ATCR25 short talk 6: Orian Bricard on using TWISTAR to identify cognate cancer epitopes of a TCR of interest.

#ATCR25 short talk 5: Giancarlo Croce on using phage display screening to identify cancer-specific TCRs at the epitope level.

#ATCR25 short talk 4: Mikhail Pogorelyy on TIRTLseq for a cheaper paired TCR sequencing.

#ATCR25 short talk 3: Bjorn Kwee on the possibility that TCR-epitope prediction is poor because the underlying data has more false positives than commonly believed.

#ATCR25 short talk 2: Abi Colley on building a TCR-epitope data set capturing variability on both the TCR and epitope side to build an annotation model.

#ATCR short talk 1: Sofie Gielis on the influence of data on TCR-epitope predictions.

Fifth #ATCR25 speaker: @kischober.bsky.social on how T cell receptor avidity influences clonal expansion following antigen exposure in a "natural experiment" (vaccination)

Fourth #ATCR25 speaker: Dietmar Zehn on the formation of seemingly exhausted T cells during acute infections, with the theory that this is tied to the affinity of the TCR-pMHC interaction.