ArticleTransplantation direct2026
IL35 Production After Living-donor Renal Transplantation: Relevance to Local, Exosome-mediated, Clinical Tolerance.
Article in Transplantation direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: We previously reported that 100% of HLA-identical siblings and 50% of HLA-haploidentical donor-recipient pairs exhibited bidirectional immunoregulation (BDIR) before living-related renal transplantation. BDIR predicted successful transplant outcomes. However, at the time, we were unaware of the role of the cytokine interleukin-35 (IL35) in immunoregulation, and we now appreciate exosomes as a means of confining immunoregulation to the transplanted tissue. Here we show that HLA-identical sibling transplants use IL35 in posttransplant BDIR. Methods: We analyzed the posttransplant IL35 response using the trans-vivo delayed type hypersensitivity assay in HLA-identical sibling transplants, using anti-IL35 antibodies to block immune-regulatory function as measured by either (1) inhibition of the tetanus toxoid/diphtheria toxoid recall response or (2) uncovering of direct response, in both the donor anti-recipient and the recipient anti-donor (minor H) antigen directions. Results: We found that minor antigen-specific human regulatory T cells, known to be present in peripheral blood mononuclear cell of HLA-identical siblings pretransplant, also caused BDIR via production of IL35 posttransplant. Conclusions: We conclude that human IL35 is a component of BDIR in HLA-identical sibling transplantation. Since IL35 is one of a subclass of exosome-delivered cytokines, this means that human IL35 could sustain local BDIR within the transplant itself. It follows that local BDIR would persist indefinitely if donor leukocytes were allowed to stably engraft. This may account for the success of combined total lymphoid irradiation/bone marrow transplantation/renal transplantation induction of stable tolerance in HLA-identical sibling transplant recipients.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.