Pitää testailla tarkemmin. Voi olla että tämänkaltaiset systeemit tulevat jatkossa reviewereiden rutiinikäyttöön, joten kannattenee ajaa myös artikkelin kirjoittajan itsekriittisessä mielessä, jotta välttyisi kaikkein ilmeisimmältä kritiikiltä (jota nykyään refereet eivät välttämättä hoksaa esittää)

Kokeilin äsken juuri hyväksytyllä manullamme. Vaikutti luotettavalta ja hyvältä systeemiltä: tunnisti mielestäni hyvin keskeiset uudet havainnot ja antoi ihan adekvaattia kritiikkiä mahdollisista aukoista ja suositteli "pehmentäviä tekstikorjauksia" ja mahdollisia täydentäviä eksperimenttejä.

Many thanks to all our collaborators at Kuopio University Hospital, @varhahyvinvointi.bsky.social, @pohde.bsky.social, @utu.fi, @helsinki.fi, @unioulu.bsky.social, and to the funders of the study: Foundation for Pediatric Research, Päivikki and Sakari Sohlberg Foundation and ISLAB Laboratory Centre.

Taken together, our data supports the view that autoantibodies generated in JIA likely target either multi-molecular antigen structures (like dsDNA-nucleosome complexes) and/or posttranslationally modified nuclear proteins, possibly formed during inflammatory processes in the joints.

However, no purified antigen appears to explain this reactivity. Interestingly, around 20% of JIA patients exhibited antibody reactivity to artificial nucleosome-dsDNA complexes, but not to isolated nucleosomes or dsDNA.

We studied a large collection of plasma samples from JIA patients and age-matched controls, using a variety of both clinical-grade and exploratory autoantibody assays. We confirmed previous findings that autoantibodies in JIA appear to target chromatin structures.

Currently in Boston at +37C, luckily most of the time in air-conditioned conference halls…

Huge thanks for this big effort to all our collaborators at @uniuef.bsky.social @utu.fi @unioulu.bsky.social @helsinki.fi and to our funders: Research Council of Finland, Finnish Diabetes Research Foundation and @sigridjuselius.bsky.social

This could potentially complicate the use of cTph cells as blood biomarkers in autoimmune diseases.

Finally, we show that the CXCR5-PD1hi cells are more hererogeneous at the single cell level than CXCR5+PD1hi cells and TCR sharing is demonstrated also with CXCR5-PD1lo cells. This suggests that the putative "cTph" cells contain other T cell subsets besides those with a true Tph signature.

Second, we investigated the phenotype of cTfh and cTph using flow cytometry and single cell omics. We confirm previous studies that blood CXCR5-PD1hi (cTph) and CXCR5+PD1hi (cTfh) cells share B-cell helper features. However, no phenotypic changes are seen in T1D, just an increase in frequency.

It turns out that no changes are seen at this point, only later, i.e. a few years before clinical disease onset, and more dominantly for cTph than cTfh cells, suggesting that the increase of these cells in blood is associated with disease progression and hypothetically ectopic lymphoid structures.

Here, we addressed a few outstanding questions. First: what is the exact timing of cTfh and cTph increase during the disease process? For this, we analysed rare samples collected at the time of seroconversion, i.e. the earliest detectable time point of autoimmunity.

Links to the previous studies:

diabetesjournals.org/diabetes/art...

link.springer.com/article/10.1...

This study complements our earlier studies on the role of these "B-cell helper" T cells in T1D, where we have shown that both cTfh and cTph are increased in the blood of children with newly diagnosed T1D and also in prediabetic autoantibody-positive (AAb+) children.

There is always the Midsummer next year!

Great news, well deserved! Congratulations Eliisa!