Abstract
Type 1 diabetes (T1D) and celiac disease are both characterized by an autoimmune feature. As T1D and celiac disease share several common risk factors such as environment, genetics and immune dysregulation, patients have risk of developing the other disease subsequently. Patients with manifest T1D may have had a latent celiac disease, which is activated parallel to the anti-islet immune reactivity during the development of T1D. Contrary, a low prevalence of β-cell autoimmunity is found in young patients with celiac disease. The role of antigen-specific T cells and their relation to cytokines and chemokines is not well characterized in children with combination of T1D and celiac disease. Defective regulation and an impaired ability of responder T cells to be suppressed are suggested to contribute. We have previously shown that children suffering from these two immunological diseases in combination have a suppressed immune response to several antigens for example food antigens like gluten. Low percentages of both early and late effector memory CD8 + cells together with observations of immune aberrancies seen in the gut, in children who are prone to T1D, may suggests poor development of oral tolerance that may predispose for development of celiac disease. This review highlights the immunological complexity in these two common pediatric immunological disorders that indicates that the combination of type 1 diabetes and celiac disease is an immunological challenge. It is obvious that we are far from understanding the immunological impact of these two autoimmune diseases in combination. This immunological challenge therefore needs to be elucidated to be able to predict and prevent these autoimmune diseases.
Highlights
Citation for the original published paper: Faresjö, M. (2016) Children diagnosed with both type 1 diabetes and celiac disease - an Immunological challenge
Poor development of oral tolerance seen as immune aberrancies with low percentages of both early and late effector memory CD8+ cells in the gut of children who are prone to Type 1 diabetes (T1D) may predispose for development of celiac disease
Activation of Th1 cells by signal transducer and activator of transcription (STAT)-4 and T-box expressed in T cells (T-bet) will cause cytokine secreting of especially IFN-γ, IL-2 and tumor necrosis factor (TNF) [3, 4] and promote cell-mediated immunity for example cytotoxic and inflammatory responses mediated by macrophages, natural killer (NK) and T cells
Summary
Virus-specific CD8+ T cells produce a similar range of cytokines for example IL-2, TNF-α, GM-CSF and IFN-γ and chemokines for example CCL3, CCL4 and CCL5 as CD4+ T-cells This indicates that cytotoxic T cells can be divided into subpopulations and can obtain cytokine secreting phenotypes that require transcription factors suchlike those of helper T cells [27]. Adoptive transfer of TGF-β and IL-2 ex vivo generated CD4 T-reg cells is suggested to be a potential treatment of autoimmune diseases because these Treg cells have the functional and phenotypic properties including suppressive activity similar to natural occurring CD4CD25 cells [35]. This far, CD4+CD25hi cells with high expression of CD39, CD101, CD129 and FoxP3 but low expression of CD45RA and CD127 may be the best way for characterization of human Treg cells
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