Peripheral blood CD4<sup>+</sup> and CD8<sup>+</sup> T cell type 1 and type 2 cytokine production in atopic asthmatic and normal subjects

Cho, Sang Heon; Stanciu, Luminita A.; Begishivili, T.; Bates, P. J.; Holgate, Stephen T.; Johnston, Sebastian L.

doi:10.1046/j.1365-2222.2002.01281.x

Cited by 67 publications

(56 citation statements)

References 43 publications

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“…Thus, IFN-c-producing Th1-type cells detected in peripheral blood of atopic patients have been suggested to also play a role in asthma [35,36], especially during the symptomatic phases of the disease. It could be hypothesised that a Th2 orientation in asthma mainly characterises the immune response during the sensitisation process and the acute reaction to allergen exposure; whereas, chronic inflammation could be underlined by a less specific T-cell profile.…”

Section: Discussionmentioning

confidence: 99%

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

Pilette¹,

Francis²,

Till³

et al. 2004

Eur Respir J

124

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T-helper (Th) 2 cytokines are thought to mediate most features of allergic inflammation in atopic asthma. However, it remains unclear whether chemokine pathways direct selective recruitment of Th2 cells to the airways during human allergic responses.Bronchoalveolar lavage (BAL) was performed in 15 nonsmoking mild atopic asthmatics before and 24 h after a fibreoptic segmental allergen challenge, and chemokines related to T-cell recruitment were assayed by ELISA.The Th2-related C-C chemokine (CCR)4 ligands, macrophage-derived chemokine/C-C chemokine ligand (CCL)22 and thymus and activation-regulated chemokine/CCL17, were increased in BAL after challenge. These chemokines correlated significantly with lymphocyte numbers and with interleukin (IL)-5 and IL-13 in post-challenge BAL. In contrast, two out of three putative Th1-related chemokines did not change. There were no alterations in monokine induced by interferon (IFN)-c/CXC chemokine ligand (CXCL)9 or macrophage inflammatory protein-1a/CCL3; whereas a significant increase in IFN-induced protein-10kDa/CXCL10 was observed, which did not correlate with the T-cell influx. In peripheral mononuclear cells from atopic donors, CCL22 and CCL17 were induced by IL-4 and IL-13, further supporting the relationship between CCL22/CCL17 and Th2 cytokines. Finally, CCL22 was able to trigger actin polymerisation in peripheral CD4z T-cells expressing CCR4.Thus, C-C chemokine receptor 4 ligands are up-regulated in the airways of atopic asthmatics following allergen exposure, contribute to the T-cell influx to the airways and are closely related to the Th2-cytokine response.

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Section: Discussionmentioning

confidence: 99%

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

Pilette¹,

Francis²,

Till³

et al. 2004

Eur Respir J

124

View full text Add to dashboard Cite

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“…Most infections induce asthma exacerbation and a T helper (Th) 1 inflammatory response. Some studies have shown that some Th1 cells are present in asthmatic patients, which could be related to bronchial hyperreactivity (Krug et al 1996;Magnan et al 2000;Cho et al 2002). Interferon-c (IFN-c), produced by Th1 cells, exerts an inhibitory effect on Th2 cells and has extensive and diverse immunoregulatory effects on various cells (Chung and Barnes 1999).…”

Section: Introductionmentioning

confidence: 99%

Association between genetic variation in the gene for death-associated protein-3 (DAP3) and adult asthma

et al. 2004

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Lung epithelium plays a central role in modulation of the lung inflammatory response, and lung repair and airway epithelial cells are targets in asthma and viral infection. Activated T lymphocytes release cytokines such as interferon-gamma (IFN-c) that induce apoptosis, or programmed cell death, of damaged epithelial cells. Death-associated protein-3 (DAP3) is involved in mediating IFN-c-induced cell death. To assess the possible involvement of genetic variants of DAP3 with asthma, we searched for single-nucleotide polymorphisms (SNPs) in the gene and conducted a case-control study with 1,341 subjects. We found a strong association between bronchial asthma (BA) in adults (P=0.0051, odds ratio=1.87, 95% CI=1.20-2.92), whereas no association was found with childhood asthma. The tendency was more prominent in patients with higher serum total immunoglobulin E (IgE) (>250 IU/ml) (P=0.00061, odds ratio=2.40, 95% CI=1.44-4.00). DAP3 was expressed in normal bronchial epithelial cells, and the expression was induced by IFN-c. These results indicated that specific variants of the DAP3 gene might be associated with the mechanisms responsible for adult BA and contribute to airway inflammation and remodeling.

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“…ϩ T cells can produce many cytokines, including IFN-␥, as well as IL-4 and IL-5, after induction (24,51), and a classification of these CD8 ϩ cells into a Tc1 subset (producing Th1-like cytokines) and a Tc2 subset (producing Th2-like cytokines) has been proposed (26).…”

Section: Discussionmentioning

confidence: 99%

Cytokine Profiles in Adult Mink Infected with Aleutian Mink Disease Parvovirus

Jensen¹,

Castelruiz²,

Aasted³

2003

J Virol

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The aim of this study was to examine the levels of gamma interferon (IFN-␥)-, interleukin 4 (IL-4)-, and IL-8-producing cells in peripheral blood mononuclear cells from mink infected with the Aleutian mink disease parvovirus (ADV). As expected, ADV-infected mink developed high plasma gamma globulin values (hypergammaglobulinemia) and enhanced quantities of CD8-positive (CD8؉ ) cells in the blood during the infection. We quantified the percentages of IFN-␥-and IL-4-positive lymphocytes and IL-8-positive monocytes up to week 38 after virus challenge. The results clearly indicated marked increases in the percentages of IFN-␥-and IL-4-producing lymphocytes during ADV infection. The total number of IL-8-producing monocytes in the blood of ADV-infected mink stayed fairly constant during the infection. In order to characterize the phenotype of the cytokine-producing cells, we performed double-labeling fluorescence-activated cell sorter (FACS) experiments with CD8 surface labeling in one channel and cytokine intracellular staining in the other. We found that most IFN-␥ and IL-4 in ADV-infected mink was produced by CD8؉ cells, while in the uninfected mink, these cytokines were primarily produced by a cell type that was not CD8 (possibly CD4-positive cells). We also observed that IL-8 was almost exclusively produced by monocytes. All of the above findings led us to conclude that both Th1-and Th2-driven immune functions are found in mink plasmacytosis.Aleutian mink disease (AD), also known as mink plasmacytosis, is a common and economically important disease in mink. It is caused by a persistent infection with Aleutian mink disease virus (ADV), a nondefective parvovirus (16). In newborn mink, ADV infection may cause atypical interstitial pneumonia (10). This was observed just 20 years ago (34). The classical (adult) form of AD was described in 1956 by Hartsough and Gorham (30), and the disease is characterized by development of hypergammaglobulinemia (plasmacytosis), elevated levels of CD8-positive (CD8 ϩ ) lymphocytes, viral persistency, and immune complex formation (1,2,15,44). The most common pathological findings are glomerulonephritis and arteritis, and severely affected mink often die of renal failure (44). ADV cannot be neutralized in vivo despite the presence of very high concentrations in serum of antibody to virus capsid proteins (8,45). In fact, antibody-mediated enhancement of infection has been observed in connection with ADV infection (3,14,15,32,43). With regard to the identity of the in vivo ADV replicating cell(s) it is generally agreed that the virus-permissive cells probably are Fc receptor-positive cells (7,11,15,32).There is only one existing report on cytokine levels during ADV infection (15). Using reverse transcription-PCR technology, this study reported higher interleukin 6 (IL-6) mRNA levels in lymph nodes from ADV-infected mink (10 and 60 days after infection) than from uninfected mink. It also found biologically active IL-6 in supernatants from short-term lymph node cultures from ADV-infected mi...

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Peripheral blood CD4⁺ and CD8⁺ T cell type 1 and type 2 cytokine production in atopic asthmatic and normal subjects

Cited by 67 publications

References 43 publications

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

Association between genetic variation in the gene for death-associated protein-3 (DAP3) and adult asthma

Cytokine Profiles in Adult Mink Infected with Aleutian Mink Disease Parvovirus

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Peripheral blood CD4+ and CD8+ T cell type 1 and type 2 cytokine production in atopic asthmatic and normal subjects

Cited by 67 publications

References 43 publications

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge

Association between genetic variation in the gene for death-associated protein-3 (DAP3) and adult asthma

Cytokine Profiles in Adult Mink Infected with Aleutian Mink Disease Parvovirus

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Peripheral blood CD4⁺ and CD8⁺ T cell type 1 and type 2 cytokine production in atopic asthmatic and normal subjects