Characterization of Regulatory T Cells in Patients Infected by Leishmania Infantum .
Rephany F PeixotoBruna M GoisMarineuma MartinsPedro Henrique de Sousa PalmeiraJuliana C RochaJuliana de Assis Silva GomesFátima L A A AzevedoRobson Cavalcante VerasIsac A de MedeirosTeresa C S L GrisiDemétrius A M de AraújoIan P G AmaralTatjana de Souza Lima KeesenPublished in: Tropical medicine and infectious disease (2022)
High IL-10 levels are pivotal to parasite survival in visceral leishmaniasis (VL). Antigenic stimuli induce IL-10 expression and release of adenosine by CD39/CD73. Due their intrinsic ability to express IL-10 and produce adenosine from extracellular ATP, we evaluated the IL-10, CD39, and CD73 expression by Regulatory T cells (Treg) correlated with VL pathology. Using flow cytometry, Treg cells was analyzed in peripheral blood samples from VL patients (in the presence and absence of Leishmania infantum soluble antigen (SLA)) and healthy individuals (negative endemic control-NEC group), without any treatment. Additionally, IL-10 levels in leukocytes culture supernatant were measured in all groups by ELISA assay. VL patients presented more Treg frequency than NEC group, independently of stimulation. ELISA results demonstrated that SLA induced higher IL-10 expression in the VL group. However, the NEC group had a higher Treg IL-10 + compared to the VL group without stimulation and SLA restored the IL-10 in Treg. Additionally, an increase in Treg CD73 + in the VL group independently of stimuli compared to that in the NEC group was observed. We suggest that Treg are not the main source of IL-10, while the CD73 pathway may be an attempt to modulate the exacerbation of immune response in VL disease.
Keyphrases
- regulatory t cells
- end stage renal disease
- ejection fraction
- newly diagnosed
- chronic kidney disease
- immune response
- peripheral blood
- poor prognosis
- dendritic cells
- flow cytometry
- prognostic factors
- chronic obstructive pulmonary disease
- cell proliferation
- high throughput
- binding protein
- induced apoptosis
- inflammatory response
- drug induced
- extracorporeal membrane oxygenation
- toll like receptor
- endoplasmic reticulum stress