John Chan
Rutgers University-New Brunswick, NJ·Microbiology & Immunology
Tuberculosis kills by provoking the immune system into damaging the very organ it is defending. When *Mycobacterium tuberculosis* (Mtb) infects the lung, immune cells wall off the bacteria inside clumps called granulomas.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Genetics
- Topics
tuberculosis
Mtb
granuloma
- Grants
- 2 known grants, through Jul 2030
What they work on
- Determine how B cells drive lung inflammation in chronic tuberculosis, testing whether they expand CD4+ helper T cells and interferon-gamma responses while suppressing the anti-inflammatory signal IL-10, using B cell-deficient, knockout and transgenic mouse strains.
- Characterize the B cell clumps that ring necrotic and cavitary lung lesions in people with chronic TB, using archived human TB tissues with multiplex immunofluorescence, RNAscope gene-expression imaging, single-cell RNA sequencing and spatial transcriptomics.
- Test whether IL-10 signaling controls granulomatous lung inflammation by shaping CD4+ T cells and antigen-presenting cells, using IL-10 pathway blockade in Mtb-infected mice.
- Test the hypothesis that Rv2623, a stress protein switched on during Mtb dormancy, restrains the putative cell wall exporter Rv1747 through a phosphothreonine-237 contact, using biochemical binding assays and point-mutant bacterial strains.
- Define how levels of PIMs, immune-modulating cell wall glycolipids, determine Mtb's fate in an infected host, by building isogenic mutants that make graded amounts of PIMs and comparing their growth and virulence in animal infection models.
More about the research
Granulomas help contain the infection, but in long-running disease they can turn destructive, killing lung tissue and carving out cavities. Cavities that open into the airways fill with oxygen-rich air, letting bacteria multiply to enormous numbers and spread to other people by coughing; survivors can be left with permanently reduced lung function even after drugs cure the infection. Work in this lab approaches this problem from two directions: which immune cells drive the damaging inflammation, and which bacterial genes let the pathogen slow its own growth and persist quietly inside a host.
Why it matters
Tuberculosis remains a major global health burden, and the lung damage it causes both fuels transmission through cavity formation and leaves survivors with lasting breathing problems. Identifying how B cells and the anti-inflammatory signal IL-10 drive that damage could point to treatments that spare lung tissue and reduce spread, while mapping the Rv2623–Rv1747–PIM pathway may explain how the bacterium stays dormant and suggest drug targets against persistent infection.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Russell Kempker
Emory University, GA·Medicine & Clinical Research·Early-career
Identify the metabolic and lipid profiles of each region of human necrotic lung granulomas, using MALDI-2 mass spectrometry imaging and laser capture microdissection on surgically removed TB lung tissue.
Mushtaq Ahmed
University of Chicago, IL·Microbiology & Immunology
Determine whether bone morphogenetic protein (BMP) signaling, a lung development and repair pathway, is required to control Mycobacterium tuberculosis and prevent reactivation of latent TB.
Bree Aldridge
Weill Medical College of Cornell University, NY·Microbiology & Immunology
Generate single-cell profiles of Mycobacterium tuberculosis responding to drug treatment and to gene knockdown, working with the four program projects on the treatments and genes each one studies.
The school
Rutgers University-New Brunswick: 57 labs on PI Pages, $837M a year on research, 713 research doctorates a year.
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