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Ari Molofsky

@arimolofskylab.bsky.social

Professor of Laboratory Medicine, UCSF. Tissue Immunology researcher. Neuroimmunology. Stromal immunology. Clinical Pathology and Hematopathology. Mentor, doctor, educator, lifelong learner.

1,168 Followers  |  124 Following  |  2 Posts  |  Joined: 15.11.2024  |  1.6416

Latest posts by arimolofskylab.bsky.social on Bluesky

Type 1 immune response reduces seizure risk after traumatic brain injury Nature Reviews Immunology - A preprint by Mroz et al. reports a role for IFNgamma in protecting against seizures after traumatic brain injury.

NEW @preprintclub.bsky.social Journal Club by Jennifer Ahn & @jengommerman.bsky.social highlighting a @biorxiv-immuno.bsky.social paper by @arimolofskylab.bsky.social, Jeanne Paz and colleagues that reports a role for IFNg in protecting against seizures after traumatic brain injury

05.03.2025 09:15 โ€” ๐Ÿ‘ 12    ๐Ÿ” 5    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0
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#standupforscience2025

08.03.2025 16:44 โ€” ๐Ÿ‘ 13    ๐Ÿ” 0    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0

Agree! An honor to receive the Bowes award together with @kampmann.bsky.social - a testament to the incredible collaborations at @ucsfhealth.bsky.social that make our science possible!

07.03.2025 22:44 โ€” ๐Ÿ‘ 22    ๐Ÿ” 4    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 1

The study section I sit on (Innate Immunity B) will be rescheduled to April.
Just putting this out there since folks have been getting no notifications about whats going on with their grants.

01.03.2025 01:18 โ€” ๐Ÿ‘ 113    ๐Ÿ” 21    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 0
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3/ With a single IV injection, Ark313 achieves gene delivery in up to 25% of T cells, in both circulating and tissues, including tissue resident memory! This unlocks new possibilities for studying T cell function in their natural niche. (๐Ÿ™ to Roberto Ricardo Gonzalez and @arimolofskylab.bsky.social)

04.02.2025 20:50 โ€” ๐Ÿ‘ 2    ๐Ÿ” 1    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 0

Cool perspective on the role of brain extracellular matrix!

17.01.2025 19:37 โ€” ๐Ÿ‘ 0    ๐Ÿ” 0    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0
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In Nov '24: ILC2s promoted formation of inhibitory synapses during a period of postnatal brain development in mice. This influenced social behaviour in the adult mice.

https://buff.ly/49yODYd

From @annamolofskylab.bsky.social and @arimolofskylab.bsky.social et al
#Neuroimmunology @science.org

11.12.2024 17:28 โ€” ๐Ÿ‘ 14    ๐Ÿ” 4    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0
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, TNFฮฑ 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.

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, TNFฮฑ 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 ๐ŸŽ…! Our paper on how the ๐Ÿซ 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. ๐Ÿงช #Immunosky 1/9

06.12.2024 22:37 โ€” ๐Ÿ‘ 295    ๐Ÿ” 83    ๐Ÿ’ฌ 29    ๐Ÿ“Œ 9
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Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. I...

ok- sci bsky - trying this out. our latest paper with @arimolofskylab.bsky.social shows that "allergic" immune cells (ILC2s) have a healthy function in developing brain: formation of inhibitory synapses - key tuners of brain activity www.science.org/stoken/autho...

17.11.2024 00:45 โ€” ๐Ÿ‘ 49    ๐Ÿ” 16    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 0

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