The role of HIF-1 alpha in myeloid cell inflammation

Sarah Walmsley; KA Cadwallader; ER Chilvers

doi:10.1016/j.it.2005.06.007

The role of HIF-1 alpha in myeloid cell inflammation

Sarah Walmsley, KA Cadwallader, ER Chilvers^*

^*Corresponding author for this work

Research output: Contribution to journal › Literature review › peer-review

Abstract / Description of output

Myeloid cells are key effectors of the innate immune response, and as such are often required to migrate to, and function within, sites that are markedly hypoxic. To adapt to such oxygen deplete environments they have developed functional and survival responses that are regulated by the hypoxia-inducible factor (HIF) oxygen-sensing pathway. In this review, we describe three key aspects of HIF-dependent regulation of myeloid cell function: (i) the maintenance of ATP pools and the subsequent regulation of proinflammatory responses, (ii) the HIF-dependent inhibition of neutrophil apoptosis and (iii) the HIF-mediated regulation beta 2 integrin expression.

Original language	English
Pages (from-to)	434-439
Number of pages	6
Journal	Trends in Immunology
Volume	26
Issue number	8
DOIs	https://doi.org/10.1016/j.it.2005.06.007
Publication status	Published - Aug 2005

Keywords / Materials (for Non-textual outputs)

HYPOXIA-INDUCIBLE FACTOR-1-ALPHA
GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE
NEUTROPHIL APOPTOSIS
LEUKOCYTE ADHESION
FACTOR 1-ALPHA
FACTOR-I
TRANSCRIPTIONAL ACTIVATION
LYMPHOCYTE DEVELOPMENT
PROLYL HYDROXYLATION/
O-2 HOMEOSTASIS

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title = "The role of HIF-1 alpha in myeloid cell inflammation",

abstract = "Myeloid cells are key effectors of the innate immune response, and as such are often required to migrate to, and function within, sites that are markedly hypoxic. To adapt to such oxygen deplete environments they have developed functional and survival responses that are regulated by the hypoxia-inducible factor (HIF) oxygen-sensing pathway. In this review, we describe three key aspects of HIF-dependent regulation of myeloid cell function: (i) the maintenance of ATP pools and the subsequent regulation of proinflammatory responses, (ii) the HIF-dependent inhibition of neutrophil apoptosis and (iii) the HIF-mediated regulation beta 2 integrin expression.",

keywords = "HYPOXIA-INDUCIBLE FACTOR-1-ALPHA, GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE, NEUTROPHIL APOPTOSIS, LEUKOCYTE ADHESION, FACTOR 1-ALPHA, FACTOR-I, TRANSCRIPTIONAL ACTIVATION, LYMPHOCYTE DEVELOPMENT, PROLYL HYDROXYLATION/, O-2 HOMEOSTASIS",

author = "Sarah Walmsley and KA Cadwallader and ER Chilvers",

year = "2005",

month = aug,

doi = "10.1016/j.it.2005.06.007",

language = "English",

volume = "26",

pages = "434--439",

journal = "Trends in Immunology",

issn = "1471-4906",

publisher = "Elsevier",

number = "8",

}

TY - JOUR

T1 - The role of HIF-1 alpha in myeloid cell inflammation

AU - Walmsley, Sarah

AU - Cadwallader, KA

AU - Chilvers, ER

PY - 2005/8

Y1 - 2005/8

N2 - Myeloid cells are key effectors of the innate immune response, and as such are often required to migrate to, and function within, sites that are markedly hypoxic. To adapt to such oxygen deplete environments they have developed functional and survival responses that are regulated by the hypoxia-inducible factor (HIF) oxygen-sensing pathway. In this review, we describe three key aspects of HIF-dependent regulation of myeloid cell function: (i) the maintenance of ATP pools and the subsequent regulation of proinflammatory responses, (ii) the HIF-dependent inhibition of neutrophil apoptosis and (iii) the HIF-mediated regulation beta 2 integrin expression.

AB - Myeloid cells are key effectors of the innate immune response, and as such are often required to migrate to, and function within, sites that are markedly hypoxic. To adapt to such oxygen deplete environments they have developed functional and survival responses that are regulated by the hypoxia-inducible factor (HIF) oxygen-sensing pathway. In this review, we describe three key aspects of HIF-dependent regulation of myeloid cell function: (i) the maintenance of ATP pools and the subsequent regulation of proinflammatory responses, (ii) the HIF-dependent inhibition of neutrophil apoptosis and (iii) the HIF-mediated regulation beta 2 integrin expression.

KW - HYPOXIA-INDUCIBLE FACTOR-1-ALPHA

KW - GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE

KW - NEUTROPHIL APOPTOSIS

KW - LEUKOCYTE ADHESION

KW - FACTOR 1-ALPHA

KW - FACTOR-I

KW - TRANSCRIPTIONAL ACTIVATION

KW - LYMPHOCYTE DEVELOPMENT

KW - PROLYL HYDROXYLATION/

KW - O-2 HOMEOSTASIS

U2 - 10.1016/j.it.2005.06.007

DO - 10.1016/j.it.2005.06.007

M3 - Literature review

SN - 1471-4906

VL - 26

SP - 434

EP - 439

JO - Trends in Immunology

JF - Trends in Immunology

IS - 8

ER -

The role of HIF-1 alpha in myeloid cell inflammation

Abstract / Description of output

Keywords / Materials (for Non-textual outputs)

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