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@immunologypodcast.comSep 29, 2026, 4:42 PM

πŸ€” Curious about cellular crosstalk between #immune cells and surrounding tissues?

Then stay tuned for next week's episode featuring Dr. Merav Cohen at Tel Aviv University, where we deep dive into decoding interactions using single-cell technologies!

Her latest work: https://bit.ly/47dxYck

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@jcellsci.bsky.socialSep 29, 2026, 9:11 AM

In their Review, Ishani Sharma and Partha Roy examine the cell-intrinsic, niche-specific and #immune controls that govern #cancer dormancy transitions, and the strategies aimed at blocking relapse.
journals.biologists.com/jcs/article/...

Figure showing regulation of dormancy emergence of DTCs in the lung microenvironment. On arrival in the lung, DTCs lodge in the alveolar and perivascular niches. Dormancy is enforced by several converging cues. These include contact with AT1 lung epithelium (which promotes survival and restrains growth), anti-proliferative action of vascular endothelium-derived TSP-1, sequestration of tumor-derived ECM remodeling enzymes (e.g. LOXL2) by endothelial PEAR1, and activation of a NAS1-driven NR2F1-based dormancy transcriptional program by stromal cell-derived BMP. NR2F1 mediates suppression of Ξ”Np63, the pro-proliferative isoform of p63 (TP63). Reactivation (indicated by the proliferation marker Ki67) occurs when tumor cells interact with AT2 epithelium (which provides pro-proliferative signals). Additional reactivation cues include tumor-derived factors tenascin-C and Coco (which antagonizes BMP to release the dormancy brake via integrin-dependent FAK signaling; phosphorylated FAK is indicated as pFAK), sprouting angiogenesis (which supplies TGF-Ξ²1 and periostin), and activation of integrin-dependent ERK–MLCK signaling triggered by alterations in the ECM (e.g. fibrotic ECM and/or remodeling of laminin by NET-derived proteases like MMP9). Together, these opposing endothelial, epithelial, stromal and matrix inputs determine whether DTCs remain dormant or undergo metastatic outgrowth in the lung. Created in BioRender by Sharma, I., 2026. https://BioRender.com/j23rlwk. This figure was sublicensed under CC-BY 4.0 terms.
@allermd.bsky.socialSep 28, 2026, 5:58 PM

Moderate-to-severe #chronic #spontaneous #urticaria is associated with increased risk of #immune-#mediated #diseases: A population-based study. Open Access. ivancevichmd.blogspo...

Moderate-to-severe #chronic #spontaneous #urticaria is associated with increased risk of #immune-#mediated #diseases: A population-based study. Open Access.  https://ivancevichmd.blogspot.com/2026/09/moderate-to-severe-chronic-spontaneous.html
@klytron.bsky.socialSep 28, 2026, 9:01 AM

Your immune system runs billions of generative simulations every second. No design, just pure evolutionary engineering. Learn more at klytron.com #science #biology #evolution #klytron

#science #biology #evolution #klytron #immune

@sablesystems.bsky.socialSep 25, 2026, 4:15 PM

How do #immune cells and #inflammation contribute to #obesity?

With help from Promethion Core #Metabolic Cages, scientists characterized #metabolic health and #obesity risk in #MRP8Cre transgenic mice, which are used to investigate #neutrophil biology.

buff.ly/1CpsVPN

#Metabolism #Physiology

@zenhaus.bsky.socialSep 25, 2026, 3:29 PM

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amazon.com/zenhaus

#Iodine #Immune #VitaminD

@foodnourish.bsky.socialSep 25, 2026, 8:05 AM

πŸ“£ New Podcast! "Why Grandma’s classic cold remedy with Garlic actually works" on @Spreaker #allicin #alliinase #biohacking #colds #cooking #fitness #flu #food #garlic #healing #health #holistic #immune #immunity #nutrition #prevention #remedies #science #supplements #wellness

@cleeterichter.bsky.socialSep 23, 2026, 9:26 AM

We are looking for interested and motivated Masters or Medical students to help us investigate the immunometabolic changes in #immune cells during #cachexia. Apply today and join us at the lab of @andreasbergthaler.bsky.social and @meduniwien.ac.at

pii.meduniwien.ac.at/en/our-depar...

@toppnews.bsky.socialSep 23, 2026, 2:13 AM

#biotechnology #cancer #immune cells #research #Signal #Yang
🌐 www.newsmart.ch

@zenhaus.bsky.socialSep 21, 2026, 11:45 PM

Unleash the inner hero with #Glutathione! πŸ’–

The master antioxidant is a secret weapon against daily stressors, helping you reclaim your vitality, glow and shine. πŸ₯‹

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amazon.com/zenhaus

woman meditating in grey-brown mitsy forest scene
@vanderbiltvicb.bsky.socialSep 21, 2026, 3:27 PM

How do colorectal tumors keep #immune cells out?

New #research reveals how DDR1-containing nanoparticles help create barriers that exclude immune cells, identifying a potential therapeutic #target.

Read: bit.ly/4AtOMte

More VICB publications: medschool.vanderbilt.edu/vicb/publica...

Scientific illustration comparing DDR1-low and DDR1-high tumors. DDR1-low tumors show disorganized collagen, less contractile fibroblasts, and CD8+ T cells entering the tumor. DDR1-high tumors release supermeres enriched in DDR1, increasing fibroblast contraction and collagen alignment to form a barrier that prevents CD8+ T cells from penetrating the tumor.
@allermd.bsky.socialSep 18, 2026, 4:14 PM

#Nasal #Epithelial #Immune #Signatures Are Associated With #Age-#Dependent #Asthma #Trajectories in Early Life. Open Access. ivancevichmd.blogspo...

#Nasal #Epithelial #Immune #Signatures Are Associated With #Age-#Dependent #Asthma #Trajectories in Early Life. Open Access. https://ivancevichmd.blogspot.com/2026/09/nasal-epithelial-immune-signatures-are.html#more
@plosbiology.orgSep 18, 2026, 1:01 PM

Most #bacterial #immune systems raise an alarm when they sense a #phage. This Primer explores a @plosbiology.org study showing how type II Panoptes reverses this logic by maintaining a quiet signal & sensing infection through its sudden disappearance πŸ§ͺ Paper: buff.ly/1ixwg9v Primer: buff.ly/WmnHZBp

Type II Panoptes inverts the logic of nucleotide signaling in bacterial immunity. Top: In type III CRISPR-Cas, Cas10 synthesizes cyclic oligoadenylates (cAn) only upon infection; the signal binds and activates a CARF effector, arresting growth. Type II Panoptes does the reverse. Its mCpol enzyme produces cA3 constitutively at low levels, and this signal keeps the CARF-TM effector repressed. Infection is sensed not as the appearance of a signal, but as its disappearance: when phage enzymes (Acb1 given as an example) deplete cA3, the effector is released and growth arrests. Bottom: Because Acb1 evolved to disable cyclic-nucleotide defenses such as type III CRISPR, a phage carrying it strips cA3 as collateral damage and triggers Panoptes. A phage lacking Acb1 avoids this trap but remains vulnerable to CRISPR. Together, the two systems could impose an evolutionary trade-off on the phage.
@talius2.bsky.socialSep 18, 2026, 6:31 AM

A single #IV treatment #retrains #immune cells to fight #autoimmune diseases in early trial

Researchers developed a revolutionary IV drip that delivers engineered viruses to reprogram immune cells in the body, eliminating complex CAR-T manufacturing
scitechupdates.com/a...

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@plosbiology.orgSep 17, 2026, 12:55 PM

Acute #infections have been linked to #cancer progression, but they can also elicit #AntiTumor immune responses. This study explores gaps in understanding how infections differentially skew #immune programs to promote or restrain cancer progression @plosbiology.org πŸ§ͺ buff.ly/QfAWXBo

Upper left – healthy lung with a rare dormant cancer cell (green). Lower right – lung after infection with respiratory virus, showing expansion of dormant cancer cells (green cells; pink nucleus indicates active cell cycling). Image credit: Michael DeGregori.
@plosbiology.orgSep 17, 2026, 8:05 AM

Most #bacterial #immune systems raise an alarm when they sense a #phage. This Primer explores a @plosbiology.org study showing how type II Panoptes reverses this logic by maintaining a quiet signal & sensing infection through its sudden disappearance πŸ§ͺ Paper: buff.ly/1ixwg9v Primer: buff.ly/WmnHZBp

Type II Panoptes inverts the logic of nucleotide signaling in bacterial immunity. Top: In type III CRISPR-Cas, Cas10 synthesizes cyclic oligoadenylates (cAn) only upon infection; the signal binds and activates a CARF effector, arresting growth. Type II Panoptes does the reverse. Its mCpol enzyme produces cA3 constitutively at low levels, and this signal keeps the CARF-TM effector repressed. Infection is sensed not as the appearance of a signal, but as its disappearance: when phage enzymes (Acb1 given as an example) deplete cA3, the effector is released and growth arrests. Bottom: Because Acb1 evolved to disable cyclic-nucleotide defenses such as type III CRISPR, a phage carrying it strips cA3 as collateral damage and triggers Panoptes. A phage lacking Acb1 avoids this trap but remains vulnerable to CRISPR. Together, the two systems could impose an evolutionary trade-off on the phage.
@plosbiology.orgSep 17, 2026, 7:55 AM

R1-32-like public #antibodies drive #SARSCoV2 #virus to acquire #SpikeProtein mutations that promote #immune escape. This study characterises 4 such antibodies, showing that they acquire tolerance to SARS-CoV-2 antigenic drift via somatic hypermutation @plosbiology.org πŸ§ͺ buff.ly/iy4qUOe

Structures of mutation-tolerant antibodies in complex with SARS-CoV-2 BA.4/5 S-trimer and ACE2. Top: Cryo-EM densities of BA.4/5 S-R/6P S-trimer bound to Fab and ACE2 at 3:3:3 molar ratio. C092, C807, BD56-104, and BD56-597 Fabs, NTD, RBD, and ACE2 are colored in magenta, blue, cyan, and dark green, respectively; the rest of the S-trimer is colored in gray. The 3 RBDs in β€œup” positions are indicated, each simultaneously engaging both ACE2 and antibody. Bottom: Cryo-EM densities of BA.4/5 S1 bound to Fab and ACE2. C092, C807, BD56-104, and BD56-597 Fab-HC, Fab-LC, NTD, RBD, and ACE2 are colored in magenta, purple, blue, cyan, and dark green, respectively; the rest of the S1 is colored in gray.
@plosbiology.orgSep 16, 2026, 4:30 PM

Acute #infections have been recently linked to #cancer progression, but they can also elicit #AntiTumor immune responses. This study explores gaps in understanding how infections differentially skew #immune programs to promote or restrain cancer progression @plosbiology.org πŸ§ͺ buff.ly/QfAWXBo

Upper left – healthy lung with a rare dormant cancer cell (green). Lower right – lung after infection with respiratory virus, showing expansion of dormant cancer cells (green cells; pink nucleus indicates active cell cycling). Image credit: Michael DeGregori.
@plosbiology.orgSep 16, 2026, 4:25 PM

R1-32-like public #antibodies drive #SARSCoV2 #virus to acquire #SpikeProtein mutations that promote #immune escape. This study characterises four such antibodies, showing that they acquire tolerance to SARS-CoV-2 antigenic drift via somatic hypermutation @plosbiology.org πŸ§ͺ buff.ly/iy4qUOe

Structures of mutation-tolerant antibodies in complex with SARS-CoV-2 BA.4/5 S-trimer and ACE2. Top: Cryo-EM densities of BA.4/5 S-R/6P S-trimer bound to Fab and ACE2 at 3:3:3 molar ratio. C092, C807, BD56-104, and BD56-597 Fabs, NTD, RBD, and ACE2 are colored in magenta, blue, cyan, and dark green, respectively; the rest of the S-trimer is colored in gray. The 3 RBDs in β€œup” positions are indicated, each simultaneously engaging both ACE2 and antibody. Bottom: Cryo-EM densities of BA.4/5 S1 bound to Fab and ACE2. C092, C807, BD56-104, and BD56-597 Fab-HC, Fab-LC, NTD, RBD, and ACE2 are colored in magenta, purple, blue, cyan, and dark green, respectively; the rest of the S1 is colored in gray.
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