Daniel L. Barber, PhD

@danbarberphd.bsky.social

Immunologist. Major focus is on T cell responses to Mycobacterium tuberculosis infection.

Important paper by Björn Corleis. For decades a central tenet of #tuberculosis immunology has that IFNγ-driven iNOS expression in macrophages is the primary mechanism of bacterial control. Turns out this is really only in mice and maybe cattle. It’s not true in most species including humans an NHP.

bioRxiv Immunology@biorxiv-immuno.bsky.social · 7mo ago

Species-specific iNOS expression distinguishes epithelial and myeloid IFNγ responses in tuberculosis https://www.biorxiv.org/content/10.64898/2026.01.11.697682v1

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!

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

Kat Mayer-Barber,PhD@mayerbarber.bsky.social · 2y ago

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

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.

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.

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.

science.org

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

bioRxiv Immunology@biorxiv-immuno.bsky.social · 2y ago

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication https://www.biorxiv.org/content/10.1101/2024.03.27.586885v1