Interleukin-2 and lymphocyte-induced eosinophil proliferation and survival in asthmatic patients

Yang, Jian; Renzi, Paolo

doi:10.1016/0091-6749(93)90199-p

Cited by 16 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…reported that IL‐2 was a potent chemoattractant for EOS [6]. A number of other investigators did not, however, find any direct effect of IL‐2 on EOS migration, but showed that it acts by stimulating T cells to produce increased amounts of IL‐5 [23–27]. The contradiction between our results and those of Rand et al.…”

Section: Discussioncontrasting

confidence: 99%

Interleukin‐2 inhibits eosinophil migration but is counteracted by IL‐5 priming

Lampinen

Håkansson

2001

Clin Experimental Allergy

View full text Add to dashboard Cite

Conflicting data on the role of interleukin-2 in the recruitment of eosinophil granulocytes (EOS) to sites of inflammation have been presented. The objective of the present study was to investigate the effect of recombinant human IL-2 and anti-IL-2 on the migration of purified blood EOS. Neutralizing antibodies to IL-2 were added to a cytokine mixture with significant eosinophil chemotactic activity (ECA), and afterwards the ECA was tested on EOS from both normal and allergic donors. EOS migration was measured by a modification of the Boyden technique, using a 48-well microchemotaxis chamber. Recombinant human IL-2 was either added to the lower compartment of the chemotaxis chamber, or to the EOS for a pre-incubation period of 20 min, before migration assays towards the chemotaxins were performed. Anti-IL-2 caused a significant increase of EOS migration towards the cytokine mixture. Pre-incubation of the EOS with rhIL-2 inhibited the chemotaxis towards RANTES, PAF, IL-8 and eotaxin, and EOS migration towards IL-2 was lower than that towards buffer. These effects were more pronounced on EOS from normal than from allergic donors. Priming of the EOS with IL-5 prevented the inhibitory effect of IL-2. We hypothesize that IL-2 acts as an autocrine regulator of EOS migration, and that this inhibitory effect may be downregulated in allergy, allowing an increased migration of EOS towards chemotactic factors.

show abstract

Section: Discussioncontrasting

confidence: 99%

Interleukin‐2 inhibits eosinophil migration but is counteracted by IL‐5 priming

Lampinen

Håkansson

2001

Clin Experimental Allergy

View full text Add to dashboard Cite

show abstract

“…Neutrophil content in AT was not significantly different between WT and ob / ob mice (Figure S2D-F). While both eosinophils and neutrophils have been shown to have some proliferative capacity outside of the bone marrow (Bjornson et al, 1985; Yang and Renzi, 1993), we failed to detect any EdU incorporation into these cells within AT (Figure S2C and F). Our results suggest that obesity does not stimulate proliferation of all cells in the AT, but selectively stimulates proliferation of specific cell types including macrophages.…”

Section: Results-discussionmentioning

confidence: 70%

Local Proliferation of Macrophages Contributes to Obesity-Associated Adipose Tissue Inflammation

et al. 2014

View full text Add to dashboard Cite

SUMMARY Adipose tissue (AT) of obese mice and humans accumulates immune cells, which secrete cytokines that can promote insulin resistance. AT macrophages (ATMs) are thought to originate from bone marrow-derived monocytes, which infiltrate the tissue from the circulation. Here we show that a major fraction of macrophages unexpectedly undergo cell division locally within AT, as detected by Ki67 expression and 5-ethynyl-2′-deoxyuridine incorporation. Macrophages within the visceral AT (VAT), but not those in other tissues, including liver and spleen, displayed increased proliferation in obesity. Importantly, depletion of blood monocytes had no impact on ATM content, while their proliferation in situ continued. Treatment with monocyte chemotactic protein 1 (MCP-1) induced macrophage cell division in AT explants, while MCP-1 deficiency in vivo decreased ATM proliferation. These results reveal that proliferation in situ driven by MCP-1 is an important process by which macrophages accumulate in the VAT in obesity, in addition to blood monocyte recruitment.

show abstract

“…Blood lymphocytes have an uninhibited proliferative response to IL-2 in asthmatics (6), and when stimulated with IL-2 they release factors that increase eosinophil proliferation from progenitors and prolong eosinophil survival. whereas such an effect is not observed when lymphocytes from normal subjects are stimulated (7). We have previously shown in rats that IL-2 causes several of the lung physiologic and histologic changes observed in asthmatics.…”

mentioning

confidence: 89%

“…Stimulation of membrane receptors for IL-2 causes lymphocyte proliferation (6) and also promotes the secretion of other lymphokines that affect cellular proliferation and activation (7). In humans, interleukin-2-receptor-positive lymphocytes are increased in the blood and airways of asthmatics (7)(8)(9). and IL-2 and its mRNA are increased in lung lavage (10,11).…”

mentioning

confidence: 99%

Effects of depletion of cells bearing the interleukin-2 receptor on immunoglobulin production and allergic airway responses in the rat.

Renzi¹,

Yang²,

Diamantstein³

et al. 1996

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Lymphocytes, key cells in chronic inflammation, are increased in the airways of asthmatics and have increased expression of the interleukin-2 (IL-2) receptor, a sign of activation. We determined the effects of depleting cells bearing IL-2 receptors on immunoglobulin (Ig) production, airway inflammation, and airway responses after antigen challenge of Brown Norway rats that were sensitized to ovalbumin (OA). Both control and ART-18 (antirat IL-2 receptor) antibodies inhibited plasma specific IgE and the early (ER) and late (LR) airway responses to antigen when given from zero to 14 d after sensitization. When ART-18 was administered from 4 to 14 d after sensitization and compared with control animals, it inhibited OA specific IgE production from Day 21 onward, but it increased total IgE and specific IgG. These changes followed a significant increase in blood CD4+ lymphocytes (%) in ART-18-treated animals 14 d after sensitization. The same protocol of administration did not affect Ig levels at 14 d, but it decreased neutrophil influx into the lungs 8 h after antigen challenge without any effects on the ER and LR. Administration of ART-18 at the time of antigen challenge did not affect the subsequent airway inflammation or the increased responsiveness to methacholine that occurs 32 h after antigen challenge. In summary, depletion of IL-2-receptor-bearing cells affects lymphocyte subsets and immunoglobulin production and it decreases the influx of neutrophils into the lungs 8 h after OA challenge, but it does not significantly inhibit the ER, LR, or increased airway responsiveness after antigen challenge.

show abstract

Interleukin-2 and lymphocyte-induced eosinophil proliferation and survival in asthmatic patients

Cited by 16 publications

References 33 publications

Interleukin‐2 inhibits eosinophil migration but is counteracted by IL‐5 priming

Interleukin‐2 inhibits eosinophil migration but is counteracted by IL‐5 priming

Local Proliferation of Macrophages Contributes to Obesity-Associated Adipose Tissue Inflammation

Effects of depletion of cells bearing the interleukin-2 receptor on immunoglobulin production and allergic airway responses in the rat.

Contact Info

Product

Resources

About