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Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling

The Journal of immunology (1950), 2011-07, Vol.187 (2), p.911-918

2011

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Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

The Journal of clinical investigation, 2011-11, Vol.121 (11), p.4446-4461

2011

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The myeloid receptor PILRβ mediates the balance of inflammatory responses through regulation of IL-27 production

PloS one, 2012-03, Vol.7 (3), p.e31680-e31680

2012

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A paradoxical role for myeloid-derived suppressor cells in sepsis and trauma

Molecular medicine (Cambridge, Mass.), 2011-03, Vol.17 (3-4), p.281-292

2011

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Chronic granulomatous disease

Current opinion in immunology, 2003-10, Vol.15 (5), p.578-584

2003

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MyD88-dependent expansion of an immature GR-1(+)CD11b(+) population induces T cell suppression and Th2 polarization in sepsis

The Journal of experimental medicine, 2007-06, Vol.204 (6), p.1463-1474

2007

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Modulation of Paired Immunoglobulin-Like Type 2 Receptor Signaling Alters the Host Response to Staphylococcus aureus-Induced Pneumonia

Infection and Immunity, 2010-03, Vol.78 (3), p.1353-1363

2010

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Regulation of Phagocyte Oxygen Radical Production by the GTP-Binding Protein Rac 2

Science (American Association for the Advancement of Science), 1991-12, Vol.254 (5037), p.1512-1515

1991

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Focus on FOCIS: The continuing diagnostic challenge of autosomal recessive chronic granulomatous disease

Clinical immunology (Orlando, Fla.), 2008-08, Vol.128 (2), p.117-126

2008

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Myeloid DAP12-associating lectin (MDL)-1 regulates synovial inflammation and bone erosion associated with autoimmune arthritis

The Journal of experimental medicine, 2010-03, Vol.207 (3), p.579-589

2010

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Hematologically Important Mutations: The Autosomal Recessive Forms of Chronic Granulomatous Disease (First Update)

Blood cells, molecules, & diseases, 2000-10, Vol.26 (5), p.561-565

2000

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Cofilin undergoes rapid dephosphorylation in stimulated neutrophils and translocates to ruffled membranes enriched in products of the NADPH oxidase complex. Evidence for a novel cycle of phosphorylation and dephosphorylation

Histochemistry and cell biology, 1997-09, Vol.108 (3), p.221-233

1997

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Monoclonal antibody CL5 recognizes the amino terminal domain of human phagocyte flavocytochrome b558 large subunit, gp91phox

European journal of haematology, 2005-04, Vol.74 (4), p.337-347

2005

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Hematologically Important Mutations: X-Linked Chronic Granulomatous Disease (Second Update)

Blood cells, molecules, & diseases, 2001, Vol.27 (1), p.16-26

2001

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A Paradoxical Role for Myeloid-Derived Suppressor Cells in Sepsis and Trauma

Molecular medicine (Cambridge, Mass.), 2011-03, Vol.17 (3-4), p.281-292

2011

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Chronic granulomatous disease mutations and the PX domain

Nature cell biology, 2002-05, Vol.4 (5), p.E110-E110

2002

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Molecular quality control machinery contributes to the leukocyte NADPH oxidase deficiency in chronic granulomatous disease

Biochimica et biophysica acta, 2002-04, Vol.1586 (3), p.275-286

2002

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A Variant X-linked Chronic Granulomatous Disease Patient (X91+) with Partially Functional Cytochrome b(∗)

The Journal of biological chemistry, 1995-04, Vol.270 (14), p.8194-8200

1995

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Absolute Requirement for GTP in Activation of Human Neutrophil NADPH Oxidase in a Cell-Free System: Role of ATP in Regenerating GTP

Proceedings of the National Academy of Sciences - PNAS, 1992-03, Vol.89 (6), p.2494-2498

1992

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Unusual polyclonal anti-gp91 peptide antibody interactions with X-linked chronic granulomatous disease-derived human neutrophils are not from compensatory expression of Nox proteins 1, 3, or 4

European journal of haematology, 2005-03, Vol.74 (3), p.241-249

2005

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Unusual polyclonal anti-gp91phox peptide antibody interactions with X-linked chronic granulomatous disease-derived human neutrophils are not from compensatory expression of Nox proteins 1, 3, or 4

European journal of haematology, 2005-03, Vol.74 (3), p.241-249

2005

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Identification of a novel NCF-1 (p47-phox) pseudogene not containing the signature GT deletion: significance for A47 degrees chronic granulomatous disease carrier detection

Blood, 2002-09, Vol.100 (5), p.1845

2002

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Activation of Human Neutrophil NADPH Oxidase by Phosphatidic Acid or Diacylglycerol in a Cell-free System

The Journal of biological chemistry, 1999-08, Vol.274 (32), p.22243-22250

1999

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The Myeloid Receptor PILR[beta] Mediates the Balance of Inflammatory Responses through Regulation of IL-27 Production.(Research Article)

PloS one, 2012-03, Vol.7 (3), p.e31680

2012

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4 Primary immunodeficiency mutation databases

Advances in Genetics, 2001, Vol.43, p.103-188

2001

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Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling

Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

The myeloid receptor PILRβ mediates the balance of inflammatory responses through regulation of IL-27 production

A paradoxical role for myeloid-derived suppressor cells in sepsis and trauma

Chronic granulomatous disease

MyD88-dependent expansion of an immature GR-1(+)CD11b(+) population induces T cell suppression and Th2 polarization in sepsis

Modulation of Paired Immunoglobulin-Like Type 2 Receptor Signaling Alters the Host Response to Staphylococcus aureus-Induced Pneumonia

Regulation of Phagocyte Oxygen Radical Production by the GTP-Binding Protein Rac 2

Focus on FOCIS: The continuing diagnostic challenge of autosomal recessive chronic granulomatous disease

Myeloid DAP12-associating lectin (MDL)-1 regulates synovial inflammation and bone erosion associated with autoimmune arthritis

Hematologically Important Mutations: The Autosomal Recessive Forms of Chronic Granulomatous Disease (First Update)

Cofilin undergoes rapid dephosphorylation in stimulated neutrophils and translocates to ruffled membranes enriched in products of the NADPH oxidase complex. Evidence for a novel cycle of phosphorylation and dephosphorylation

Monoclonal antibody CL5 recognizes the amino terminal domain of human phagocyte flavocytochrome b558 large subunit, gp91phox

Hematologically Important Mutations: X-Linked Chronic Granulomatous Disease (Second Update)

A Paradoxical Role for Myeloid-Derived Suppressor Cells in Sepsis and Trauma

Chronic granulomatous disease mutations and the PX domain

Molecular quality control machinery contributes to the leukocyte NADPH oxidase deficiency in chronic granulomatous disease

A Variant X-linked Chronic Granulomatous Disease Patient (X91+) with Partially Functional Cytochrome b(∗)

Absolute Requirement for GTP in Activation of Human Neutrophil NADPH Oxidase in a Cell-Free System: Role of ATP in Regenerating GTP

Unusual polyclonal anti-gp91 peptide antibody interactions with X-linked chronic granulomatous disease-derived human neutrophils are not from compensatory expression of Nox proteins 1, 3, or 4

Unusual polyclonal anti-gp91phox peptide antibody interactions with X-linked chronic granulomatous disease-derived human neutrophils are not from compensatory expression of Nox proteins 1, 3, or 4

Identification of a novel NCF-1 (p47-phox) pseudogene not containing the signature GT deletion: significance for A47 degrees chronic granulomatous disease carrier detection

Activation of Human Neutrophil NADPH Oxidase by Phosphatidic Acid or Diacylglycerol in a Cell-free System

The Myeloid Receptor PILR[beta] Mediates the Balance of Inflammatory Responses through Regulation of IL-27 Production.(Research Article)

4 Primary immunodeficiency mutation databases

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