Andrea Ramirez García

Mexico

Determinaton of different subpopulatons of innate lymphoid cells (ILCs) in adipose tissue from healthy subjects and subjects with dyslipidemia.

Andrea Ramírez1, Esthey Layseca1, Adriana Monsiváis1

1. Immunolgy Department, Autonumus University of San Luis Potosi, San Luis Potosi, Mexico

Abstract

Background

An important risk factor for cardiovascular disease is dyslipidemia. This condition is characterized by persistent low-grade vascular inflammation and permanent hyperactivation of the innate immune system. ILCs have recently been identified in adipose tissue, where they have been implicated in the dysregulation of this tissue and atherosclerosis.

Methods

This is a cross-sectional descriptive study using convenience sampling, involving 21 subjects who underwent surgery at a private plastic and reconstructive surgery clinic. The subjects were divided into two groups, with and without dyslipidemia, according to their lipid profile. Adipose tissue samples were processed to obtain mononuclear cells for analysis by flow cytometry. Which underwent dimensional reduction using the tSNE algorithm and automatic clustering using a self-organizing map algorithm to analyze high-dimensional data

Results

Three metaclusters were obtained, from which the expression percentages of the different markers used were identified. The self-organizing map algorithm allowed us to identify the organization of the ILC subpopulations. ILC1 showed greater structural variability, while ILC2 and ILC3 remained conserved. The tSNE algorithm showed the presence of the three ILC subpopulations in the group of subjects with dyslipidemia and healthy subjects. ILC1 had a prevalence of 24.5% and 30%; ILC2 of 3.2% and 3.7%; and finally, ILC3 of 61% and 58% in subjects with dyslipidemia and healthy subjects, respectively.

Conclusions

When evaluating the phenotype, it suggests that dyslipidemia promotes an inflammatory process derived from IFNy-secreting ILC1, which seeks to be counteracted by IL-5-secreting ILC3. Although the ILC1 subpopulation is observed in healthy subjects, the compensatory effect of ILC3 was found to be absent, which could suggest that in the absence of dyslipidemia, ILC1 cells do not have relevant inflammatory activity.