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Sinclair, C.

Publications and source records attributed to Sinclair, C..

2 recordsLinked to original sources

A linear ontogeny accounts for the development of naive, memory and tumour-infiltrating regulatory T cells in mice

Foxp3+ Regulatory T cells (Treg) are a subset of CD4+ T cells that play critical functions in maintaining tolerance to self antigens and suppressing autoimmunity, regulating immune responses to pathogens and have a role in the pathophysiology of anti-tumoural immunity. Treg ontogeny is complex since they are generated following recognition of self antigens in the thymus during normal T cell development (thymic Treg), but are also induced from mature conventional T cells when activated by foreign antigen with appropriate additional cues (inducible Treg). How these distinct ontogenic pathways contribute to the maintenance and function of the mature Treg compartment in health and disease remains unclear. Here, we use a combination of fate mapping approaches in mice to map the ontogeny of Treg subsets throughout life and estimate rates of production, loss and self-renewal. We find that naive and effector/memory (EM) Treg subsets exhibit distinct dynamics but are both continuously replenished by de novo generation throughout life. Using an inducible Foxp3-dependent Cre fate reporter system, we show that naive Treg and not conventional T cells, are the predominant precursors of EM Treg in adults. Tonic development of new EM Treg is not influenced by foreign antigens from commensals, rather suggesting a role for self recognition. To investigate the ontogeny of Treg development in malignant disease, we used the same fate reporter systems to characterise the Treg infiltrate of three different model tumours. In all three cases, we found that Treg derived from pre-existing, EM Treg. Together, these results reveal a predominantly linear pathway of Treg development from thymic origin to EM Treg associated with pathophysiology of malignant disease, that is driven by self antigen recognition throughout.

immunology↗

Skeletal muscle MRI differentiates SBMA and ALS and correlates with disease severity

ObjectiveTo investigate the use of muscle MRI for the differential diagnosis and as a disease progression biomarker for two major forms of motor neuron disorders, spinal bulbar muscular atrophy (SBMA) and amyotrophic lateral sclerosis (ALS).\n\nMethodsWe applied quantitative 3-point Dixon and semi-quantitative T1-weighted and STIR imaging to bulbar and lower limb muscles and performed clinical and functional assessments in ALS (n=21) and SBMA (n=21) patients, alongside healthy controls (n=16). Acquired images were analyzed for the presence of fat infiltration or edema as well as specific patterns of muscle involvement. Quantitative MRI measurements were correlated with clinical parameters of disease severity in ALS and SBMA.\n\nResultsQuantitative imaging revealed significant fat infiltration in bulbar (p<0.001) and limb muscles in SBMA compared to controls (thigh: p<0.001; calf: p=0.001), identifying a characteristic pattern of muscle involvement. In ALS, semi-quantitative STIR imaging detected marked hyperintensities in lower limb muscles, distinguishing ALS from SBMA and controls. Lastly, MRI measurements correlated significantly with clinical scales of disease severity in both ALS and SBMA.\n\nConclusionsOur findings show that muscle MRI differentiates between SBMA and ALS and correlates with disease severity, supporting its use as a diagnostic tool and biomarker for disease progression. This highlights the clinical utility of muscle MRI in motor neuron disorders and contributes to establish objective outcome measures, which is crucial for the development of new drugs.

neuroscience↗