Inflammatory and Immunological parameters in adults with Down syndrome

Abstract

BackgroundThe increase in life expectancy within the general population has resulted in an increasing number of elderly adults, including patients with Down syndrome (DS), with a current life expectancy of about 50 years. We evaluate the parameters of humoral and cellular immune response, the quantitative expression of the regulator of calcineurin1 gene (RCAN1) and the production of cytokines. The study group consisted of adults DS (n = 24) and a control group with intellectual disability without Down syndrome (ID) (n = 21) and living in a similar environmental background. It was evaluated serology, immunophenotyping, the quantitative gene expression of RCAN1 and the production of cytokines.ResultsIn the DS group, the results showed an increase in NK cells, CD8, decreased CD19 (p < 0.05) and an increase spontaneous production of IFNgamma, TNFalpha and IL-10 (p < 0.05). There was not any difference in RCAN1 gene expression between the groups.ConclusionsThese data suggest a similar humoral response in the two groups. The immunophenotyping suggests sign of premature aging of the immune system and the cytokine production show a proinflammatory profile.

miRNA-155 upregulation and complement factor H deficits in Down’s syndrome

“…While the clinical presentation of Down’s is complex and variable, characteristic features such as progressive mental deterioration, increased risk for autoimmune disease, and early onset Alzheimer disease support the hypothesis that Down’s syndrome is associated with premature aging and abnormalities in the innate immune response [2–7]. Early genetic and bioinformatics analysis suggested that much of the developmental pathology of Down’s syndrome can be attributed to the extra chromosome 21 ‘gene dosage’ effect, resulting from the 50% increase in expression of the ~300 chromosome genes, that leads to an imbalance of critical gene expression, which in turn initiates the Down’s phenotype [2–3]. More current genetic evidence suggests that the Down’s phenotype is most likely multi-genetic, and only a specific subset of the 300 or so trisomic genes, interacting with other disomic genes, mediates disease onset [4,5].…”

Cytokine Profiles in Pericardial Effusion in a Down Syndrome Infant with Transient Abnormal Myelopoiesis

“…Trotta et al (2011) reported a spontaneous increase in the production of IFN-γ, TNF-α, and IL-10 in adult patients with DS. Nateghi Rostami et al (2012) found high levels of TNF-α and IFN-γ and low levels of IL-10 in patients with DS.…”

“…Some characteristics of cytokine production in patients with DS have been described (Shimada et al 2007;Trotta et al 2011;Nateghi Rostami et al 2012 DOL, day of life; TNF-α,tumor necrosis factor α; GM-CSF, granulocyte-macrophage colony-stimulating factor; G-CSF, granulocyte colony stimulating factor; MCP-1, monocyte chemotactic protein 1; MIP-1β, macrophage inflammatory protein 1β. a The unit of concentration of cytokines, chemokines and growth factors is all pg/mL in this Table. b The control group included 8 newborn patients who were admitted to the NICU with various risks.…”

Towards a ‘systems’-level understanding of the nervous system and its disorders

“…Specifically, the onset and the progression of CNS disease states is often characterized by deregulation of systemic and CNS-specific T- and B-cells and microglia, CNS resident mononuclear phagocytes, and associated inflammatory cascades [25-30]. One particularly intriguing study recently highlighted the importance of proper microglial functioning in the brain.…”