Malaghan Institute of Medical Research
@malaghan.bsky.social
82 followers 85 following 5 posts
New Zealand's world-class independent biomedical research institute, focusing on breakthrough discoveries in immunology and immunotherapy. Charity Reg. CC 10357
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malaghan.bsky.social
The Malaghan’s Dr Lisa Connor spoke with RNZ's Ruth Hill about the extraordinary potential of mRNA technology – from infectious disease, cancer and autoimmune diseases to rare conditions – and why New Zealand’s role is more vital than ever.
US funding cuts make NZ vaccine research more critical
Fortunately, New Zealand now has the capacity to develop home-grown vaccines, through the mRNA Platform, which has received $70m in government funding.
www.rnz.co.nz
malaghan.bsky.social
The Malaghan Institute has been awarded three Health Research Council grants, totalling $7.4M over five years, to improve cancer immunotherapies, protect vulnerable populations from measles outbreaks and investigate new therapeutic targets for eczema
Cancer, measles and allergic disease research funded in latest HRC grants round
www.malaghan.org.nz
Reposted by Malaghan Institute of Medical Research
linterman.bsky.social
Fantastic to have Johanne Jacobsen at @malaghan.bsky.social this week presenting her beautiful work on germinal centre T cells, in all their complexity.
Reposted by Malaghan Institute of Medical Research
babrahaminst.bsky.social
Postdoc Theresa Pankhurst is redefining leadership! As a Kia Niwha Leader Fellow, she is exploring leadership through the lens of Māori history, culture, and perspectives. “Leadership takes many forms,” she says—and she’s proving it every day 🙌
#IWD2025 @linterman.bsky.social @malaghan.bsky.social
Image shows Theresa Pankhurst. Text reads: Theresa Pankhurst, Honorary research fellow. Te Niwha Infestious Diseases Platform Kia Niwha Leader Fellow
Reposted by Malaghan Institute of Medical Research
rsjpalmer.bsky.social
Had a great time presenting my poster at ASI2024 Sydney Australia! We’re studying how the lung’s cellular landscape shifts during infection and influences future infections, using high-dimensional flow cytometry to profile and characterise pulmonary cells at steady state and during infection! 🫁
malaghan.bsky.social
Prof Kjesten Wiig has been appointed Director of the Malaghan Institute as Professor Graham Le Gros continues in a leadership capacity as Deputy Chair of the Trust Board and advisor to the new Director @grahamlegros.bsky.social
Kjesten Wiig appointed Director of Malaghan Institute as Graham Le Gros steps into new role
www.malaghan.org.nz
Reposted by Malaghan Institute of Medical Research
kerryhilligan.bsky.social
Super privileged to have been apart of this amazing tour-de-force study from @pauljbaker.bsky.social, @mayerbarber.bsky.social and team showing how inflammatory history of the 🫁 alters susceptibility to #covid19.
Congrats team!! 🎉🎉
mayerbarber.bsky.social
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.