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IL-15 controls T cell functions through its influence on CD30 and OX40 antigens in Celiac Disease
N Periolo1, L Guillén1, M L Arruvito1
1Instituto de Inmunología, Genética y Metabolismo, Hospital de Clínicas "José de San Martín", Universidad de Buenos Aires, Buenos Aires, Argentina.
Insights
Interleukin-15 (IL-15) uniquely promotes regulatory T cell survival in celiac disease patients. This cytokine also influences T cell responses, potentially contributing to the type I immune bias observed in celiac disease.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Celiac disease (CD) involves aberrant immune responses in the small intestine.
- T cell activation and function are central to CD pathogenesis.
- Interleukin-15 (IL-15) plays a critical role in T cell homeostasis and immunity.
Purpose of the Study:
- To investigate the role of IL-15 in modulating T cell functions in celiac disease.
- To examine the influence of IL-15 on CD30 and OX40 expressing T cells in peripheral blood and duodenal mucosa.
- To assess the impact of IL-15 on regulatory T cell phenotypes and cytokine production in CD.
Main Methods:
- Peripheral blood and duodenal biopsies were collected from celiac disease patients and healthy controls.
- Mononuclear cells and mucosal lymphocytes were treated with IL-15 and analyzed for cell surface and intracellular antigens.
- Flow cytometry was used to evaluate the expression of OX40, CD30, Foxp3, IFN-γ, and IL-4.
Main Results:
- IL-15 treatment enhanced the survival of regulatory T cells expressing OX40 in celiac disease patients.
- Celiac patients exhibited higher frequencies of IFN-γ-producing CD3+CD30+ T blasts compared to controls.
- IL-15 increased CD3+CD30+ lamina propria lymphocytes but not OX40+ lymphocytes or intraepithelial lymphocytes.
Conclusions:
- IL-15 demonstrates a novel function in controlling OX40+ regulatory T cells in celiac disease.
- Elevated IFN-γ production by CD3+CD30+ cells in celiac disease may contribute to a type I immune response.
- Understanding IL-15's role provides insights into T cell dysregulation in celiac disease.
Aim:
To evaluate the ability of interleukin (IL)-15 to control T cell functions through its influence on CD30 and OX40 expressing cells in Celiac Disease (CD). In peripheral blood (PB), by examining the expression of OX40 in conventional effectors cells and T cells with a phenotypic specialization of regulatory cells [CD4+CD25high forkhead box protein 3 (Foxp3)+], and the co stimulation of IFN-γ and IL-4 production within CD30 and OX40 positive subsets of T cells. At the duodenal mucosa, by assessing the expression of CD30 and OX40 in intraepithelial (IE) and lamina propria (LP) lymphocytes (IEL, LPL).
Patients And Methods:
PB and duodenal mucosal biopsies were obtained from 38 patients with classic CD (Cel) and 38 healthy controls (HC). Analysis of cell surface and/or intracellular antigens was performed in anti-CD3-treated PB mononuclear cells (PBMC) before and after treatment with recombinant IL-15 (rIL-15), and in IE and LP cellular suspensions prepared from duodenal biopsies pre-treated with/without rIL-15.
Results:
A subpopulation of CD3+OX40+ T blasts was induced in Cel and HC by a 3days treatment of PBMC with anti-CD3 and decreased its size thereafter, regardless of the presence of rIL-15. However, the addition of rIL-15 to T blasts distinctively induced the survival of T cells with a regulatory phenotype that expresses OX40 antigen in Cel (p<0.05). Celiac patients showed higher frequencies of IFN-γ-producing CD3+CD30+ blasts before and after treatment with rIL-15 (p<0.05, vs. HC). IL-15 increased the frequencies of CD3+CD30+ LPL (HC: p<0.05, Cel: p<0.05) but not of CD3+OX40+ LPL, and CD30 or OX40 positive IEL.
Conclusions:
The distinctive control of OX40+ cells with a T regulatory phenotype mediated by the influence of IL-15 comes out as new function of this cytokine in the context of CD. The higher production of IFN-γ by a subpopulation of peripheral CD3+CD30+ cells contributes to the type I biased immune response.
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