Lindsay Celada
Baylor College of Medicine, TX·Microbiology & Immunology
Sarcoidosis is a lung disease in which immune cells clump into small nodules called granulomas. Some patients recover, but others progress to pulmonary fibrosis — permanent lung scarring — and that progression is what kills them.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Physiology
- Topics
sarcoidosis
pulmonary fibrosis
interstitial lung disease
- Grants
- 1 known grant, through Mar 2030
What they work on
- Determine the molecular pathways that control the T cell origin and maturation of CD8 intraepithelial T lymphocytes (CD8 IELs) in the lung, including the gene network found enriched in sarcoidosis that inhibits their maturation.
- Test whether MHC class II-restricted CD8 IELs become pathogenic and drive scarring, by tracking antigen-specific, tissue-resident CD8 IELs and their responses to fibrosis in transgenic mouse models of sarcoidosis-like granulomatous disease.
- Define the gene signature and T cell receptor repertoire of CD8 IELs in pulmonary sarcoidosis, using transcriptomic and flow cytometric analysis of human lung tissue digests and airway brushings.
- Model how CD8 IELs interact with the airway lining by co-culturing human T cells with bronchial organoids in a 3D system, to test their capacity to initiate and modulate innate and adaptive immune responses.
More about the research
No one knows what triggers the disease, and the field is still divided over whether it is primarily a chronic inflammatory or an autoimmune condition. Most research has looked at active, early disease and at helper T cells, leaving fibrosis and the role of killer CD8 T cells largely unexamined.
Why it matters
Patients with sarcoidosis die mainly when the disease advances to pulmonary fibrosis, yet the drivers of that progression are unknown and current therapies do not target them. Identifying a lung-resident CD8 T cell population that can either protect against or promote scarring could point to markers that flag patients at risk and to immune pathways that might be targeted to halt progression.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ellen Robey
University of California-Berkeley, CA·Microbiology & Immunology
Define the molecular links between different branches of T cell receptor (TCR) signaling and the transcription factor network that specifies the CD4 helper fate, guided by a high-resolution single-cell map of T cell development.
James B Mclachlan
Tulane University of Louisiana, LA·Microbiology & Immunology
Determine how intradermal immunization with the detoxified enterotoxin adjuvant dmLT combined with bacterial outer membrane vesicles directs vaccine-specific T cells to mucosal tissues, tracked with MHC class I and II tetramers.
Hussein Sultan
Washington University in St Louis, MO·Microbiology & Immunology
Determine how the EBI3 subunit of the suppressive cytokine IL-35 drives induction of Tr1 regulatory CD4 T cells, using IL-35 reporter mice in established tumor models to identify which cells produce it.
The school
Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.
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