Functional Expression of IL-9 Receptor by Human Neutrophils from Asthmatic Donors: Role in IL-8 Release

Abdelilah, Soussi Gounni; Latifa, Koussih; Nutku, Esra; Cameron, Lisa; Lamkhioued, Bouchaïb; Nicolaides, Nicholas C.; Levitt, Roy C.; Hamid, Qutayba

doi:10.4049/jimmunol.166.4.2768

Cited by 62 publications

(40 citation statements)

References 43 publications

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“…In support of the involvement of IL9R in allergic diseases, a specific IL9R haplotype appears to protect against wheezing in boys [30]. In addition, it has been shown that IL9R is expressed in samples from asthmatic airways but not those from normal subjects [31][32][33].…”

Section: Par1/par2 and Diseasementioning

confidence: 95%

The Human Pseudoautosomal Region (PAR): Origin, Function and Future

Mangs¹,

Morris

2007

197

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Abstract:The pseudoautosomal regions (PAR1 and PAR2) of the human X and Y chromosomes pair and recombine during meiosis. Thus genes in this region are not inherited in a strictly sex-linked fashion. PAR1 is located at the terminal region of the short arms and PAR2 at the tips of the long arms of these chromosomes. To date, 24 genes have been assigned to the PAR1 region. Half of these have a known function. In contrast, so far only 4 genes have been discovered in the PAR2 region. Deletion of the PAR1 region results in failure of pairing and male sterility. The gene SHOX (short stature homeobox-containing) resides in PAR1. SHOX haploinsufficiency contributes to certain features in Turner syndrome as well as the characteristics of Leri-Weill dyschondrosteosis. Only two of the human PAR1 genes have mouse homologues. These do not, however, reside in the mouse PAR1 region but are autosomal. The PAR regions seem to be relics of differential additions, losses, rearrangements and degradation of the X and Y chromosome in different mammalian lineages. Marsupials have three homologues of human PAR1 genes in their autosomes, although, in contrast to mouse, do not have a PAR region at all. The disappearance of PAR from other species seems likely and this region will only be rescued by the addition of genes to both X and Y, as has occurred already in lemmings. The present review summarizes the current understanding of the evolution of PAR and provides up-to-date information about individual genes residing in this region. THE X AND Y CHROMOSOMESThe human sex chromosomes (X and Y) originate from an ancestral homologous chromosome pair, which during mammalian evolution lost homology due to progressive degradation of the Y chromosome [1]. The X-chromosome in placental mammals represents approximately 5% of the haploid genome and the gene content is almost completely conserved amongst species. To ensure dosage compensation, most genes on the X are subject to X inactivation in females. The Y chromosome is much smaller than the X, being only 2-3% of the haploid genome, and is largely composed of repeated sequences. Most genes on the Y have relatives on the X chromosome and these are not subject to X inactivation. The degeneration of the Y chromosome has been researched and reviewed extensively [2][3][4][5][6]. THE PSEUDOAUTOSOMAL REGIONSThe pseudoautosomal regions (PAR1 and PAR2) are short regions of homology between the mammalian X and Y chromosomes. The PAR behave like an autosome and recombine during meiosis. Thus genes in this region are inherited in an autosomal rather than a strictly sex-linked fashion.PAR1 comprises 2.6 Mb of the short-arm tips of both X and Y chromosomes in humans and other great apes [7,8] and is required for pairing of the X and Y chromosomes during male meiosis. All characterized genes within PAR1 escape X inactivation. X-Y pairing in the PAR is thought to serve a critical function in spermatogenesis, at least in humans and mouse [9][10][11]. PAR2 is located at the tips of the long arms and is a much shor...

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Section: Par1/par2 and Diseasementioning

confidence: 95%

The Human Pseudoautosomal Region (PAR): Origin, Function and Future

Mangs¹,

Morris

2007

197

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“…Both G-CSF and GM-CSF stimulate the mobilization and proliferation of monocytes and macrophages. [21][22][23][24][25][26][27] GM-CSF and G-CSF also have direct effects on vascular smooth muscle migration 28,29 and neutrophil activation. 22 These potentially harmful effects may outweigh the putative benefits of these agents.…”

Section: Serum Lipid Levelsmentioning

confidence: 99%

“…[21][22][23][24][25][26][27] GM-CSF and G-CSF also have direct effects on vascular smooth muscle migration 28,29 and neutrophil activation. 22 These potentially harmful effects may outweigh the putative benefits of these agents. However, because neither inflammatory markers nor macrophage infiltration of the aortic wall was increased during the early stages of atherogenesis, data from the present study do not support a primary role for altered inflammation in the observed increase in atherosclerotic lesion extent.…”

Section: Serum Lipid Levelsmentioning

confidence: 99%

Granulocyte Colony-Stimulating Factor and Granulocyte Macrophage Colony-Stimulating Factor Exacerbate Atherosclerosis in Apolipoprotein E–Deficient Mice

et al. 2007

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Background— Recent studies have suggested a potential contribution of bone marrow–derived progenitor cells to vascular repair. Preliminary clinical studies have explored the possibility that mobilization of progenitor cells with granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) can affect vascular repair. However, it is not known whether the short-term administration of G-CSF or GM-CSF exerts beneficial effects on atherosclerosis. Methods and Results— Apolipoprotein E–deficient mice were treated with either GM-CSF or G-CSF at a dose of 10 μg · kg −1 · d −1 SC administered daily for 5 days per week on alternating weeks for a total of 20 doses over an 8-week treatment period. We found that in animals maintained on a high-fat diet, both G-CSF and GM-CSF actually demonstrated an increase in atherosclerotic lesion extent. The increase in atherosclerotic extent was not associated with an increase in either inflammatory cells or expression of proinflammatory genes. Interestingly, adventitial vascularity significantly increased, suggesting a mechanistic role for vasa vasorum neovascularization. Conclusions— These findings demonstrate that in this animal model of atherosclerosis, not only did administration of G-CSF or GM-CSF fail to demonstrate any beneficial therapeutic effect, but both resulted in a worsening of atherosclerosis.

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“…They also express receptors that have been shown to be implicated in different inflammatory reactions including allergy [51, 52]. While expression of IL-9Rα was not found on PMN from normal subjects [53], expression of IL-9Rα has been observed on freshly isolated peripheral blood PMN and PMN derived from the bronchoalveolar lavage from asthmatics [54]. In that study expression of IL-9Rα protein on human PMN was widely heterogeneous.…”

Section: Effects Of Il-9 On Inflammatory Cellsmentioning

confidence: 99%

“…In that study expression of IL-9Rα protein on human PMN was widely heterogeneous. However, there was a significantly higher number of IL-9Rα+ PMN in asthmatics compared to controls [54]. Therefore expression of IL-9Rα seems to be regulated.…”

Section: Effects Of Il-9 On Inflammatory Cellsmentioning

confidence: 99%

IL-9 in Allergic Inflammation

Hauber

Bergeron

Hamid³

2004

Int Arch Allergy Immunol

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Th2 type cytokines such as interleukin (IL)-4, IL-5, IL-9, and IL-13 are important mediators in allergic inflammation. The present review will focus on the role of IL-9 in allergic inflammation. The structure and genomic architecture of IL-9 and its receptor, the source of IL-9 and its regulation as well as its effects on different cell types will be reviewed. Furthermore, the specific role of IL-9 in allergic diseases and the potential therapeutic approach of blocking IL-9 will be discussed.

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Functional Expression of IL-9 Receptor by Human Neutrophils from Asthmatic Donors: Role in IL-8 Release

Cited by 62 publications

References 43 publications

The Human Pseudoautosomal Region (PAR): Origin, Function and Future

The Human Pseudoautosomal Region (PAR): Origin, Function and Future

Granulocyte Colony-Stimulating Factor and Granulocyte Macrophage Colony-Stimulating Factor Exacerbate Atherosclerosis in Apolipoprotein E–Deficient Mice

IL-9 in Allergic Inflammation

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