Caput Local adaptation of T(reg)cells
13 important questions on Caput Local adaptation of T(reg)cells
Which markers are specific for tissue resident T cells (Trm)?
How do the Trms react normally?
Those cells are normally in steady state but seem to indicate a fast respons in several places in the body when infection occurs at specific tissue.
"Human TRMs in diverse sites exhibit increased expression of adhesion and inhibitory molecules, produce both pro-inflammatory and regulatory cytokines, and have reduced turnover compared with circulating TEM, suggesting unique adaptations for in situ immunity"
What is the role of tissue resident T cells in disease?
What is the role of Tcells in inflammatory bowel disease IBD?
Pathogenesis is multifactorial: the environment, microbioom and genetics also have influence.
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What is the difference in tcell content in the different layers of the small intestine (lamina properia and epithelial layer).
Lamina propina tcells: Tcells (more tregs than in IET) and innate cells. The tcell content resembles tcell content in the perifery.
How is homing of tcells to respectively the lymphoid tissue, vessels, lamina propina and epithelium achieved?
Which important T cell subset is recently found that has a large impact on IBD?
These cells are present in both the Intestinal Epithelia and the Lamina Propina.
Explain the compartimentalization of the CD4CD8alfaalfa T cells in the colon.
- Three types of CD4CD8 cells in LPT have a more activated transcriptional profile (more TCR signalling, more NK-kb signalling, more oxidative phospohorylation) compared to IET (1)
- IET show an immune regulatory profile (more PD-1 and LAG3 expression, negative regulators of late and early respons) compared to LPT (2)
- LPT have a more cytotoxic/Trm profile compared to IET at steady state (3)
So
CD4CD8alfaalfa cells in LPT: Cytotoxic and active.
"" in IET: Immune regulatory
Both: Trm (tissue resident memory) upregulated.
What happens when steady state is "broken" (after stimulation with pathogen)?
Which mechanisms do tregs have to supress the immune system?
- Secretion of inhibitory cytokines
- Metabolic disruption
- Cytolysis
- Targeting dendritic cells
How do Tregs adapt when inflammation occurs?
So, the micro-environment shapes the type of effector program.
What are the feautures of Tregs and Teffs in the synovial fluid of patients with Juvenile Idiopathic Arthritis (JIA; common autoimmune disease with chronic inflammation in the cells).
SF Tregs show specific upregulation of effector markers (ICOS, GITR); "effector Tregs".
In SF-JIA tregs, several pathways are upregulated compared to other Tregs, such as IFNgamma signalling, IL12 signalling etc. This indicates a Th1 signature of these Trefs.
Which specific proteins are upregulated in Tregs in JIA-SF.
In which settings is the effector profile of Tregs also upregulated?
This program is environment independent (?)
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