ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Low-Affinity Memory CD8+ T Cells Mediate Robust Heterologous Immunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- A pain from the nose to the head: neurological commitment during long COVID.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Transplantation elicits a clonally diverse CD8Cell reports · 2023Article
- What's the Catch? The Significance of Catch Bonds in T Cell Activation.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Direct In Vivo Activation of T Cells with Nanosized Immunofilaments Inhibits Tumor Growth and Metastasis.ACS nano · 2023Article
- The magnitude of LFA-1/ICAM-1 forces fine-tune TCR-triggered T cell activation.Science advances · 2022Article
- Rapid video-based deep learning of cognate versus non-cognate T cell-dendritic cell interactions.Scientific reports · 2022Article
- Critical role of the CD44Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Biomechanics of T Cell Dysfunctions in Chronic Diseases.Frontiers in immunology · 2021Review
- Relationship of 2D Affinity to T Cell Functional Outcomes.International journal of molecular sciences · 2020Review
- TCR Signal Strength and Antigen Affinity Regulate CD8Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- T-cell receptor affinity in the age of cancer immunotherapy.Molecular carcinogenesis · 2020Review
- Inhibition of SHP-1 Expands the Repertoire of Antitumor T Cells Available to Respond to Immune Checkpoint Blockade.Cancer immunology research · 2020Article
- T-cell receptor signal strength and epigenetic control of Bim predict memory CD8Cell death and differentiation · 2020Article
- miR-155 Overexpression in OT-1 CD8Molecular therapy oncolytics · 2020Article
- CD45RB Status of CD8Cell reports · 2020Article
- RIPK3 and Caspase-1/11 Are Necessary for Optimal Antigen-Specific CD8 T Cell Response Elicited by Genetically ModifiedFrontiers in immunology · 2020Article
- Tissue-resident memory T cells and their biological characteristics in the recurrence of inflammatory skin disorders.Cellular & molecular immunology · 2020Review
- CTL-Derived Exosomes Enhance the Activation of CTLs Stimulated by Low-Affinity Peptides.Frontiers in immunology · 2019Article
- Altered Binding of Tumor Antigenic Peptides to MHC Class I Affects CD8Cancer immunology research · 2018Article
- Transplantation preferentially induces a KLRG-1Transplant immunology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Heterologous immunity is recognized as a significant barrier to transplant tolerance. Whereas it has been established that pathogen-elicited memory T cells can have high or low affinity for cross-reactive allogeneic peptide-MHC, the role of TCR affinity during heterologous immunity has not been explored. We established a model with which to investigate the impact of TCR-priming affinity on memory T cell populations following a graft rechallenge. In contrast to high-affinity priming, low-affinity priming elicited fully differentiated memory T cells with a CD45RB(hi) status. High CD45RB status enabled robust secondary responses in vivo, as demonstrated by faster graft rejection kinetics and greater proliferative responses. CD45RB blockade prolonged graft survival in low affinity-primed mice, but not in high affinity-primed mice. Mechanistically, low affinity-primed memory CD8(+) T cells produced more IL-2 and significantly upregulated IL-2Rα expression during rechallenge. We found that CD45RB(hi) status was also a stable marker of priming affinity within polyclonal CD8(+) T cell populations. Following high-affinity rechallenge, low affinity-primed CD45RB(hi) cells became CD45RB(lo), demonstrating that CD45RB status acts as an affinity-based differentiation switch on CD8(+) T cells. Thus, these data establish a novel mechanism by which CD45 isoforms tune low affinity-primed memory CD8(+) T cells to become potent secondary effectors following heterologous rechallenge. These findings have direct implications for allogeneic heterologous immunity by demonstrating that despite a lower precursor frequency, low-affinity priming is sufficient to generate memory cells that mediate potent secondary responses against a cross-reactive graft challenge.
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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.