Top Tweets for #dendriticCells
Harnessing #DendriticCells for therapeutics: cancer & beyond! π
Shalin Naik, Filipe Pereira, Ira Mellman, Virginia Pascual & many more take #DC2026 from discovery to translation!
β° FINAL DAY! Late-Breaking Abstracts close TONIGHT!
Donβt miss your chance to join us π΄!
ππ
Inside the tumor: how do #DendriticCells shape cancer immunity?
Meet our #DC2026 Plenary 6 speakers Miriam Merad, Santiago Zelenay & Max Krummel!
β° Last chance! Late-Breaking Abstracts close TOMORROW, August 28!
ππ
Keep calm or fight back? How do #DendriticCells make the call at mucosal barriers?
Meet our #DC2026 Plenary 5 speakers: William Agace, Daniel Mucida & Marco Colonna!
β° Late-Breaking Abstracts are OPEN through August 28. Join the global DC community!
ππ
DCs on the move! How do #DendriticCells patrol tissues and coordinate immunity?
Meet our #DC2026 Plenary 3 speakers: Sophie Janssens, Shannon Turley & Ana-Maria Lennon-DumΓ©nil!
β° Late-Breaking Abstracts are OPEN through August 28. Join the global DC community!
ππ
One family, many functions: from identity to function in #DendriticCells!
Meet our #DC2026 Plenary 2 speakers: Dan Littman, Chrys Brown & Barbara Schraml!
β° Late-Breaking Abstracts are OPEN through August 28. Bring your latest science and join the global DC community!
ππ
Where do #DendriticCells come from, and what makes them who they are?
Meet our #DC2026 Plenary 1 speakers: Kenneth Murphy, Tomohiko Tamura & Florent Ginhoux!
β° Late-Breaking Abstracts are OPEN through August 28. Bring your latest science and join the global DC community!
ππ
Research Article by S Cai et al. (@UKEHamburg) #Glutamine #metabolism shapes the #phenotypicadaptation of #uterine #dendriticcells in response to early #allogeneicpregnancy
https://t.co/7BHJKY8Rqa
You love #DendriticCells... how could you not? π
β° Tomorrow is your last chance to register at the Early Bird rate! #DC2026
Join us this October in San Diego!
https://t.co/CK228iLNhW
π Please repost! π
@MaxKrummel @ZunigaLab
Ward, Kar, Balan, and Bhardwaj @BhardwajLab review how conventional type 1 #DendriticCells (cDC1s) coordinate antitumor immunity through cross-presentation, immune cell networking, and spatial organization in tumors. https://t.co/A77oF770ZS
#CancerFocus #Immunotherapy
Congrats to the lab of Dr. Ansuman Satpathy (@Satpathology) on their new @Cancer_Cell study! π
Using mitochondrial DNA mutations for single-cell lineage tracing, they show that tumor-associated #macrophages and #DendriticCells arise from distinct circulating monocyte clones that appear epigenetically programmed toward specific immune fates before entering tumors.
π https://t.co/lL4guBnJxF
Shared previously: Dendritic cells extend a reach into the anti-tumor response: https://t.co/koXV1q9xke
Here, Ignacio Melero & team @unav integrate 7 checkpoint inhibitor trials with spatial tissue analyses to test whether conventional type-1 #DendriticCells correlate with clinical benefit across cancers. The findings: Conventional type-1 DC density is associated with checkpoint inhibitor response across 1 multiple types of #cancer.
The figure: Multiplex immunofluorescence analyses of NSCLC samples from patients treated with immunotherapy show a positive association between cDC1 density and overall survival.
Dendritic cells extend a reach into the anti-tumor response: https://t.co/koXV1q9xke
Here, Ignacio Melero & team @unav integrate 7 checkpoint inhibitor trials with spatial tissue analyses to test whether conventional type-1 #DendriticCells correlate with clinical benefit across cancers. The findings: Conventional type-1 DC density is associated with checkpoint inhibitor response across 1 multiple types of #cancer.
The figure: Multiplex immunofluorescence analyses of NSCLC samples from patients treated with immunotherapy show a positive association between cDC1 density and overall survival.
#DendriticCells will shine in sunny #SanDiego #California this October π
You still have a couple of days to submit an abstract and be considered for a travel award, join us at #DC2026!
π¨ We heard youβ¦ so we extended the deadline!
#DC2026 submissions now close May 1
π Join the global dendritic cell community in San Diego
Submit now β donβt miss it!
https://t.co/INzFBL1xJH
@MaxKrummel @ZunigaLab π
Explore JCB's special collection of recent advances in the cell biology of immune cells, including #macrophages, #Bcells, #DendriticCells and #neutrophils.
π https://t.co/DlWCkkDmib
#AAI2026
Immunotherapy Enhanced by Restoring Mitochondrial Function in Dendritic Cells
A new metabolic mechanism describes how tumors disable βgatekeeperβ cells to prevent immune response to cancer
@StJude
#GENcancer #dendriticcells #immuneresponse
https://t.co/7YV7amnOXQ
π§ $NWBO #DCVax #Alzheimers #Aging #Immunotherapy #Neuroscience #Longevity #BrainHealth #DendriticCells #Senescenceββββββββββββββββ
The aging brain has been understood as a collection of independent pathologies: amyloid accumulation, tau propagation, microglial activation, blood-brain barrier breakdown, sleep disruption, neurotransmitter imbalance. The Immune Brain proposes that these are not independent. They are downstream consequences of a single upstream failure: the dendritic cellβs loss of IL-12p70 production capacity.
In a young brain, meningeal immune cells actively operate cognitive, motor, sensory, emotional, and autonomic functions under the direction of IL-12-competent dendritic cells. This is not theoretical. Filiano et al. demonstrated that meningeal IFN-gamma is required for social behavior. Derecki et al. showed IL-4 is required for spatial learning. SCID, nude, and Rag-knockout mice all exhibit cognitive deficits reversible by immune reconstitution. The brain runs on calibrated immune instruction, and the dendritic cell sets the calibration through IL-12p70, which functions as a biological dimmer switch.
Aging turns that switch down through three converging vicious cycles. The SASP-STAT3 axis silences IL-12 transcription in new dendritic cells through chromatin remodeling and CDK9 blockade. The Delneste feed-forward loop diverts monocyte precursors away from DC fate entirely. And the HPA-cortisol axis, driven by senescent microglia in the hypothalamus producing chronic NF-kB activation, suppresses IL-12 through glucocorticoid receptor-mediated chromatin and mitochondrial damage. Critically, the glucocorticoid receptor physically binds STAT3 to form a transactivating complex that co-drives C/EBP-beta, the master emergency myelopoiesis transcription factor. The SASP loop and the cortisol loop are not parallel. They converge on the same molecular complex in the bone marrow.
The alpha-DC1, manufactured ex vivo on the EDEN bioreactor platform, escapes every suppressive lock aging installs. The Kalinski maturation cocktail (TNF-alpha, IL-1-beta, IFN-gamma, IFN-alpha, poly-I:C, without PGE2) produces 10-60 times more IL-12p70 than standard DCs while installing the mitochondrial fitness state (OPA1-NRF1 signaling, high TMRM) that You et al. identified as the master determinant of cDC1 function. Subcutaneous injection in the arm captures senescent cell antigens at the injection site, instructs T cells with full IL-12 brightness in the draining lymph node, and generates brain-homing effectors through four anatomical routes including the recently discovered skull bone marrow-meningeal vascular channels that are resistant to age-related decline.
The frameworkβs most consequential claim is that this intervention is a true biological reboot, not chronic replacement therapy. Peripheral senescent cell clearance reduces SASP, breaking the STAT3 arm. Hypothalamic senescent microglial clearance normalizes cortisol, breaking the GR arm. Both inputs to the GR-STAT3/C/EBP-beta complex are removed simultaneously. New HSCs differentiate with balanced lymphoid-myeloid output. New DCs emerge IL-12-competent within one to two weeks, consistent with DC turnover kinetics and confirmed by the one-week IL-12 recovery observed after stress cessation in animal models. Cortisol normalization addresses three of the five epigenetic locks on HSCs (epigenetic remodeling, niche inflammation, mitochondrial dysfunction); SASP reduction addresses the remaining two. The Cushing syndrome IRIS phenomenon, where 10-17% of patients develop new-onset autoimmune disease after surgical cortisol normalization, validates the magnitude of immune reconstitution achievable through this pathway.
The sex differences literature adds a dimension that strengthens rather than challenges the framework. Five independent studies show pharmacological senolytics (D+Q, ABT-263, fisetin) consistently fail or harm females through uncontrolled SASP release from a larger senescent substrate burden. The alpha-DC1 mechanism predicts the opposite: Wilcoxen et al. demonstrated that female APCs secrete IL-12 but not IL-10 during T cell activation (a binary polarity difference reversed by castration), and Yee Mon et al. showed female CD8+ T cells have intrinsic enhanced sensitivity to IL-12, producing more granzyme B per cell division. The female immune system is already wired to the IL-12 polarity the alpha-DC1 exploits. The mode of cell death, not the sex of the patient, is the variable that determines whether senolysis helps or harms.
The Harvard Aging Brain Study anchors the clinical relevance: among 298 cognitively unimpaired elderly, higher baseline plasma IL-12p70 predicted less cognitive decline, fewer tau tangles, and less hippocampal volume loss. A 2024 meta-analysis of 3,619 patients confirmed DC vaccines improve overall survival (HR 0.71) with trial sequential analysis reaching the threshold for a true-positive result. The trial design proposes cognitively unimpaired elderly ages 65-80 with amyloid burden and low baseline IL-12p70, stratified by sex and clonal hematopoiesis status, with dual biomarker readouts (plasma IL-12p70 and salivary cortisol diurnal slope) creating a four-quadrant diagnostic matrix that identifies precisely where the mechanism succeeds or fails.
Seven novel contributions. Six falsifiable predictions with quantitative thresholds. Five operational reboot criteria. Ninety-two references. Every component independently validated. What has not been attempted is the synthesis: brain aging as a dendritic cell instructional deficit correctable by a single manufactured cell delivered by a shot in the arm.
https://t.co/kRI3sCJVaT
#DendriticCells drive immunity. Whether you study #infection, #cancer, or #Tcells, understanding DCs can enhance your research!
Join us at #DC2026 in San Diegoπ
β³ Abstracts close 4/17
π Please share
Travel awards thanks to @ImmunologyAAI @LEOFondet & Boehringer Ingelheim
Sara Monaci and colleagues identify a "Novel role of Hippo effector #YAP1 as a rheostat controlling #Inflammation in #DendriticCells"
π https://t.co/Dzr5IMbDjX
Thymic myeloid cells are heterogenous and include a novel population of transitional #DendriticCells. From MatouΕ‘ VoboΕil, Kristin Hogquist and colleagues: https://t.co/Yx3R754Ls1
π#Hematopoiesis & #Myeloid Cells collection https://t.co/Lzs4o2mlTX
#KSMyeloid26 #KSHemato26
#Radiotherapy induces YTHDF2 in #DendriticCells impairing cross-presentation and T cell function, by Chen, He, Liang, Weichselbaum et al: https://t.co/pw86XauHtN
π#Hematopoiesis & #Myeloid Cells collection https://t.co/jUrSaKyxgu
#KSMyeloid26 #KSHemato26
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