Functional assessment of CD2, CD3 and CD28 on the surface of peripheral blood T‐cells from infants at low versus high genetic risk for atopy

Holt, Patrick G.; Somerville, C.; Baron‐Hay, M. J.; Holt, Barbara J.; Sly, Peter D.

doi:10.1111/j.1399-3038.1995.tb00263.x

Cited by 10 publications

(6 citation statements)

References 13 publications

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“…The higher concentration of anti‐CD3 required for maximal proliferation in 18‐month‐old children, as compared to adults, is in agreement with previous studies in 6‐month‐old infants ( 8) and newborns ( 33). Similarly, the more rapid decline with anti‐CD3 dilution in atopic children supports the previous findings of a reduced anti‐CD3 responsiveness in infants with atopic heredity ( 8). Moreover, recent data from our group show that during the first 18 months of life, children with a double atopic heredity have a slower post‐natal rise of CD3 MFI than children with no or single atopic heredity ( 34).…”

Section: Discussionsupporting

confidence: 92%

“…Based on T‐cell studies (reviewed in 7), e.g. assessment of sheep erythrocyte rosette‐forming T‐cell numbers, phytohaemagglutinin (PHA) responsiveness, interferon‐γ (IFN‐γ) production, and anti‐CD3 responsiveness in infants with atopic heredity ( 8), it has been hypothesized that atopic children show a delayed immunological maturation after birth. CD2, the receptor for sheep erythrocytes, enhances the interaction between the major histocompatibility complex (MHC) and the T‐cell receptor via binding to leukocyte function‐associated antigen‐3 (LFA‐3) on the antigen‐presenting cell ( 9).…”

mentioning

confidence: 99%

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Expression of and responses to CD2 and CD3 in 18‐month‐old children with and without atopic dermatitis

Jenmalm¹,

Aniansson-zdolsek²,

Holt³

et al. 2000

Pediatric Allergy Immunology

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We hypothesize that atopy is associated with a reduced T-cell function early in life and an imbalance in cytokine production. The purpose of this study was to investigate the expression of and responses to CD2 and CD3 in children who did or did not develop atopic dermatitis early in life. The expression of CD2 and CD3 was analyzed by flow cytometry, and proliferation of CD2 and CD3 was studied by 3H-thymidine incorporation in phytohaemagglutinin (PHA)- and anti-CD3-stimulated peripheral blood mononuclear cells (PBMC) of 18-month-old children, 25 with and 29 without atopic dermatitis. Exogenous interleukin (IL)-2 was added to compensate for possible functional differences in accessory cells. Anti-CD3-induced secretion of IL-4, IL-5, IL-6, IL-10, IL-13, and interferon-gamma (IFN-gamma) was analyzed by enzyme-linked immunosorbent assay (ELISA). Atopy was associated with a low proportion of CD2+ lymphocytes. Responsiveness to PHA, which activates lymphocytes partly via the sheep erythrocyte receptor, CD2, was reduced in the allergic children. The anti-CD3-induced proliferation declined more rapidly with antibody dilution in the allergic than in the non-allergic children. Atopic dermatitis was associated with high levels of anti-CD3-stimulated IL-5 secretion. The IL-4/IL-10 and IL-4/ITFN-gamma ratios were higher in children with elevated total immunoglobulin E (IgE) levels. Skin prick test-negative children with eczema produced higher levels of IL-10 than skin prick test-positive children. In conclusion, atopic children have a reduced T-cell function. Atopic dermatitis is associated with increased IL-5 production, while high total IgE levels are associated with high IL-4/IFN-gamma and IL-4/IL-10 ratios.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Expression of and responses to CD2 and CD3 in 18‐month‐old children with and without atopic dermatitis

Jenmalm¹,

Aniansson-zdolsek²,

Holt³

et al. 2000

Pediatric Allergy Immunology

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“…This may indicate a delayed upregulation of the CD3 receptor in children with an atopic family history. The findings were subtle, but they are supported by observations that T–cells from infants with a family history of allergy required higher levels of anti–CD3 stimulation to reach maximum responses than adults, while low–risk infants did not differ from adults [12]. …”

Section: Discussionsupporting

confidence: 53%

Expression of the T–Cell Markers CD3, CD4 and CD8 in Healthy and Atopic Children during the First 18 Months of Life

Zdolsek

Ernerudh²,

Holt³

et al. 1999

Int Arch Allergy Immunol

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Background: There is little information available about the development of T–cell immunity in healthy and atopic children. We have studied prospectively the mean fluorescence intensity of the T–cell receptor complex–associated CD3, CD4 and CD8 in relation to atopic family history (AFH) and the development of atopic disease. Methods: Children with a defined AFH (n = 172) were followed from birth to 18 months and the cumulative history of atopic disease was recorded. Blood samples were obtained at birth and at 18 months, and in a subgroup of 78 children also at 3, 6 and 12 months. Multicolour flow cytometry was used to analyse pan T–cells (CD3+CD45+CD14–), T–helper–(CD3+CD4+) and T–cytotoxic–(CD3+CD8+) cells. Results: At 18 months, 31 children were atopic and 118 non–atopic. Children who developed atopic disease had a higher CD4 expression (mean fluorescence intensity, MFI) on CD4+CD3+ lymphocytes at birth and at 3 months, particularly as compared with non–atopic children without AFH. Furthermore, the CD3 expression on CD3+CD45+CD14– lymphocytes increased more slowly with age in children with double atopic heredity, as compared with children with no or only one atopic family member. Conclusions: The higher expression of the CD4 receptor in early infancy in children who developed atopic disease compared with non–atopics suggests a delayed expression in T–helper cells. Children with a strong AFH had a slower increase in the expression of CD3, indicating a delayed T–cell maturation.

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“…In human, the incidence of type 1 diabetes has increased during the past several decades in developed countries where environmental conditions have dramatically changed [128–131]. This hypothesis suggests that bacterial antigens would be presented by the innate immune system to the T lymphocytes very early in life supporting the notion that immunostimulation can benefit the maturation of the postnatal immune system [132, 133]. Consequently, in case of misrecognition of the bacterial antigen, the adaptive immune system will be exacerbating its aggressiveness against the pancreatic cells and destroy them.…”

Section: Gut Microbiota and Type 1 Diabetesmentioning

confidence: 99%

Gut microbiota and diabetes: from pathogenesis to therapeutic perspective

et al. 2011

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More than several hundreds of millions of people will be diabetic and obese over the next decades in front of which the actual therapeutic approaches aim at treating the consequences rather than causes of the impaired metabolism. This strategy is not efficient and new paradigms should be found. The wide analysis of the genome cannot predict or explain more than 10–20% of the disease, whereas changes in feeding and social behavior have certainly a major impact. However, the molecular mechanisms linking environmental factors and genetic susceptibility were so far not envisioned until the recent discovery of a hidden source of genomic diversity, i.e., the metagenome. More than 3 million genes from several hundreds of species constitute our intestinal microbiome. First key experiments have demonstrated that this biome can by itself transfer metabolic disease. The mechanisms are unknown but could be involved in the modulation of energy harvesting capacity by the host as well as the low-grade inflammation and the corresponding immune response on adipose tissue plasticity, hepatic steatosis, insulin resistance and even the secondary cardiovascular events. Secreted bacterial factors reach the circulating blood, and even full bacteria from intestinal microbiota can reach tissues where inflammation is triggered. The last 5 years have demonstrated that intestinal microbiota, at its molecular level, is a causal factor early in the development of the diseases. Nonetheless, much more need to be uncovered in order to identify first, new predictive biomarkers so that preventive strategies based on pre- and probiotics, and second, new therapeutic strategies against the cause rather than the consequence of hyperglycemia and body weight gain.

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Functional assessment of CD2, CD3 and CD28 on the surface of peripheral blood T‐cells from infants at low versus high genetic risk for atopy

Cited by 10 publications

References 13 publications

Expression of and responses to CD2 and CD3 in 18‐month‐old children with and without atopic dermatitis

Expression of and responses to CD2 and CD3 in 18‐month‐old children with and without atopic dermatitis

Expression of the T–Cell Markers CD3, CD4 and CD8 in Healthy and Atopic Children during the First 18 Months of Life

Gut microbiota and diabetes: from pathogenesis to therapeutic perspective

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