Abstract 083: γ/δ T Cells Play a Role in Development of Hypertension
Bibliographic record
Abstract
Objective: Both innate antigen-presenting cells and the adaptive immune system have been shown to play a role in the development of hypertension. Nevertheless, the T cell subsets involved in the pathophysiology of hypertension remains unclear. There is a small subset of “innate-like” T cells expressing the γ/δ T cell receptor (TCR) rather than the α/β TCR that could play a role bridging the innate and adaptive immune systems. We previously observed that angiotensin (Ang) II caused an increase in number and activation of γ/δ T cells and Ang II-induced systolic blood pressure (SBP) rise and vascular injury were blunted in Tcr δ -/- mice, which are devoid of γ/δ T cells. In order to further characterize the role of γ/δ T cells in hypertension, we determined whether Ang II-effects would be blunted by antibody-induced depletion of γ/δ T cells. In addition, we tested whether SBP in human could be predicted by combining the expression of genes encoding TCRGC (TCR gamma constant region) and pro-inflammatory markers of γ/δ T cells in peripheral blood mononuclear cells (PBMC). Method and Results: Thirteen to 15-week old male C57BL/6 wild-type (WT) mice were infused with Ang II (490 ng/kg/min, SC) for 14 days and injected IP with anti-γ/δ TCR or control isotype antibodies 1 day before and at day 6 of Ang II infusion. Depletion of γ/δ T cells decreased SBP (147±2 vs 167 ± 3 mm Hg, P <0.05) and restored mesenteric artery relaxation responses to acetylcholine (E max : 90±4 vs 62 ± 8%, P <0.05) compared to isotype antibody-treated mice. Using the SBP data and the PBMC gene expression profile (GSE12288) of 222 human subjects, we predicted with a supervised machine learning approach SBP by combining the gene expression of TCRGC and pro-inflammatory makers including interleukin-17A, interferon-γ and their receptors (R=0.23, P <0.001). Conclusion: Antibody-induced depletion further demonstrates the role of γ/δ T cells in Ang II-induced SBP elevation and vascular injury. Prediction of SBP using PBMC gene expression of γ/δ T cells and pro-inflammatory markers suggests that γ/δ T cells contribute to the development of human hypertension.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.004 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".