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Arkachaisri, T.

Publications and source records attributed to Arkachaisri, T..

2 recordsLinked to original sources

CyNET- a network analysis framework for high dimensionality, system level analyses of the functional Immunome

The immune system is a complex "Network of Networks", in which various immune cell subsets interact and influence each others functions, ultimately determining immune competence and the control or onset of disease. The coordinated interactions between these cell subsets determine whether the outcome is a normal physiological state or a pathological condition. Established statistical procedures largely ignore the interactions between subsets and rely on statistically significant changes in the frequency of cell subsets. We developed CyNET (Cytometry Network)-- an analysis platform based on a network science approach to understand the immune system holistically. CyNET enables us to quantify the systems level and subsets level properties. We show that changes in the centrality of the nodes (immune subsets) reflect better biological functions than changes in frequency. We used CyNET to analyze the immune development along the chronological age gradient. Peripheral blood cells from healthy newborns (cord blood), adults (20 to 55 years), and elderly (70 years and above) human subjects were further used for validation using single-cell transcriptomics. We found that network edge density, degree centralization, and assortativity score reflect the maturation and development of the immune system along the age axis, thus enabling the characterisation of the functional architecture of the Immunome and the identification of key functional hubs within the immune networks.

immunology↗

An immunome perturbation is present in juvenile idiopathic arthritis patients who are in remission and will relapse upon anti-TNFα withdrawal

ObjectivesBiologics treatment with anti-TNF is efficacious in juvenile idiopathic arthritic (JIA) patients. Despite displaying clinical inactivity during treatment, many patients will flare upon cessation of therapy. The inability to definitively discriminate patients who will relapse or continue to remain in remission after therapy withdrawal is currently a major unmet medical need. CD4 T cells have been implicated in active disease, yet how they contribute to disease persistence despite treatment is unknown.\n\nMethodsWe interrogated the circulatory reservoir of CD4+ immune subsets at the single cell resolution with mass cytometry (CyToF) of JIA patients (n=20) who displayed continuous clinical inactivity for at least 6 months with anti-TNF, and were subsequently withdrawn from therapy for 8 months, and scored as relapse or remission. These patients were examined prior to therapy withdrawal for putative subsets that could discriminate relapse from remission. We verified on a separate JIA cohort (n=16), the continued dysregulation of these circulatory subsets 8 months into therapy withdrawal. The immunological transcriptomic signature of CD4 memory in relapse/remission patients was examined with Nanostring.\n\nResultsAn inflammatory memory subset of CD3+CD4+CD45RA-TNF+ T cells deficient in immune checkpoints (PD1-CD152-) was present in relapse patients prior to therapy withdrawal. Transcriptomic profiling reveals divergence between relapse and remission patients in disease centric pathways involving (a) TCR activation, (b) apoptosis, (c) TNF, (d) NF-kB and (e) MAPK signalling.\n\nConclusionsA unique discriminatory immunomic and transcriptomic signature is associated with relapse patients and may explain how relapse occurs.

immunology↗