Daniel L. Barber, PhD

We are looking to hire post-docs to work on T cell responses to M. tuberculosis infection using murine and NHP models. If you know T cells and wanna work on the top global infectious killer check us out. BSL3 experience not required. The NIH intramural program in Bethesda MD is an amazing place!

We are looking for post-docs interested in studying T cell responses to M. tuberculosis infection…especially basic T cell immunologists who are interested in learning to work with BSL3 pathogens. The NIH intramural program is an amazing place to train!

Excited to share our last study. Huge congrats to Sarah Monard, Arnaud Métais, @gclugo.bsky.social, @chrisverollet.bsky.social and all colleagues!
We have found a mysterious cell type inside TB lung lesions that seems neuron-like but isn't quite a nerve cell.
Let's dive in👇

shorturl.at/x4Sb5

What an incredible analysis!!!

Today we report that an engineered skin bacterium, swabbed gently on the head of a mouse, can unleash a potent antibody response against a pathogen. Could lead to topical vaccines that are applied in a cream. @djenetbousbaine.bsky.social led the charge... @natureportfolio.bsky.social 1/55

Congrats Chuck!!!

Thanks to all of our amazing coauthors including @kerryhilligan.bsky.social, @danbarberphd.bsky.social for spending many, many hours tolerating me in the BSL3 lab, helping with experiments and data analysis, and providing valuable advice and moral support!

More details in this 🧵 from my powerhouse PI @mayerbarber.bsky.social whose foresight and guidance got us to this fantastic manuscript!

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication Recent or ongoing respiratory inflammation in the lung regulates antiviral immune responses to SARS-CoV-2.

Excited to share this paper from my post-doc at @niaidnews.bsky.social out now in Science Immunology! We show that recent or ongoing 🫁 infections or other pulmonary environmental exposures at the time of infection with SARSCoV2 can vastly influence early replication of the virus in mice.

Graphical summary of our paper. In mice, prior lower airway exposure to diverse inflammatory stimuli, including chronic bacterial infections such as M. tuberculosis, acute bacterial infections such as pulmonary S. aureus, viral infections such as Influenza A, type-II allergic responses such as the OVA-Alum model, activation of pulmonary TLR9 by CpG or pulmonary TLR1/2 by Pam3CSK4 leads to reduced viral burden upon subsequent infection with SARS-CoV-2 (SCV2). (2) This SCV2 restriction occurs prior to induction of SCV2-specific adaptive immune responses and is mediated through innate immune responses, including the induction of IFN-I, TNFα and IL-1 and sustained changes to the TRM (Tissue resident macrophage) cellular compartment and the pulmonary epithelium. (3) Innate cytokine and TLR signaling to both recruited immune cells and the pulmonary epithelium creates a microenvironment in the lung that limits early replication of SCV2. IFN-I signaling to pulmonary ECs (epithelial cells) increases expression of interferon-stimulated genes, that likely cell-intrinsically limit viral replication. TNF- or IL-1 suppress SCV2 independently of IFN-I signaling. TNF acts exclusively through radio-resistant cell types such as the lung epithelium, whereas IL-1 affords control both direct and indirectly, through either stromal and hematopoietic cell types, to restrict overall early SCV2 burden.

Best #Nikolaus 🎅! Our paper on how the 🫁 microenvironment can shape #innate immunity against #viruses is out @sciimmunology.bsky.social This was a herculean effort brilliantly led by @pauljbaker.bsky.social who singlehandedly established the model in the lab during the pandemic. 🧪 #Immunosky 1/9

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication Recent or ongoing respiratory inflammation in the lung regulates antiviral immune responses to SARS-CoV-2.

🙏 to @niaidnews.bsky.social, first author @pauljbaker.bsky.social and my amazing lab team, our collaborators @kerryhilligan.bsky.social @danbarberphd.bsky.social 🙏to editor extraordinaire @hannah-isles.bsky.social and the reviewers who guided us along the way 9/9
www.science.org/doi/10.1126/...

Candida auris Infections | NEJM C. auris, a serious public health threat that may have emerged because of climate change, persists on human skin and inanimate objects, frequently causing difficult-to-control outbreaks in health c...

Candida auris Infectious by Lionakis & Chowdhary in NEJM
www.nejm.org/doi/full/10....

Please add me.

Please add me.

Please add me.

As community here grows, need for starter packs will rapidly be replaced by need to curate timelines.

Enter Bluesky's custom feeds! I have made one for tuberculosis / TB posts, though it may lack specificity.

Feel free to pin & use it. Feedback welcome #IDSky #MedSky
Link👉 bsky.app/profile/did:...

Great! Thanks. Still trying to figure out how this works here.

Hi Madhu - my lab is in the NIH/NIAID intramural program and we study T cell responses to #tuberculosis.

Excited for my first post here to be our new #preprint.
👇🏻check it out below …
the recent pulmonary exposure history matters for limiting SARS-CoV-2 viral titers in the 🫁”tweetorial” to follow later