Leucocyte adhesion protein deficiency in Irish setter dogs

Trowald-Wigh, Gunilla; Håkansson, Lena; Johannisson, Anders; Norrgren, Leif; Segerstad, Carl Hård af

doi:10.1016/0165-2427(92)90050-z

Cited by 73 publications

(34 citation statements)

References 19 publications

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“…There exists an Irish Setter breed with a CD18 gene mutation that perfectly mimics the situation in humans. 40 Despite antibiosis and intensive care, puppies that are homozygous for the gene defect usually die before reaching 6 months of age. Canine models are well accepted in the field of bone marrow transplantation and results from dog studies have been directly translated into human settings.…”

Section: The Canine Lad Studymentioning

confidence: 99%

Foamy virus vectors: The usefulness of a perfect parasite

Vassilopoulos¹,

Rethwilm²

2008

Gene Ther

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Section: The Canine Lad Studymentioning

confidence: 99%

Foamy virus vectors: The usefulness of a perfect parasite

Vassilopoulos¹,

Rethwilm²

2008

Gene Ther

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“…Because CD11a, CD11b, and CD11c are the predominant ␤ 2 integrin (CD18)-associated ␣ subunits (15,37,39,53), the expression of these monomeric ␣ subunits was examined next to determine if their expression levels were a limiting factor in functional heterodimeric integrin expression. Similar to those of the ␤ integrin subunits, the expression levels of these ␣ integrin subunits did not substantially change following HCMV infection or when NF-B or PI(3)K activity was inhibited (Fig.…”

Section: Vol 81 2007 Roles Of Pi(3)k and Nf-b In Hcmv-mediated Migrmentioning

confidence: 99%

“…␤ 2 integrins can bind to the endothelial cell adhesion molecules ICAM-1 (CD11a/CD18; CD11b/CD18) and ICAM-2 (CD11a/ CD18) as well as the leukocyte adhesion molecule ICAM-3 (CD11a/CD18) (13,15). Therefore, the ␤ 1 and ␤ 2 integrins involved primarily in monocyte-endothelial interactions are CD49d/CD29, CD11a/CD18, and CD11b/CD18, although evidence also suggests that CD11c/CD18 is involved in firm adhesion to activated endothelial cells (15,37,39,53).…”

mentioning

confidence: 99%

Roles of Phosphatidylinositol 3-Kinase and NF-κB in Human Cytomegalovirus-Mediated Monocyte Diapedesis and Adhesion: Strategy for Viral Persistence

Smith

Bivins-Smith

Tilley³

et al. 2007

J Virol

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Infected peripheral blood monocytes are proposed to play a key role in the hematogenous dissemination of human cytomegalovirus (HCMV) to tissues, a critical step in the establishment of HCMV persistence and the development of HCMV-associated diseases. We recently provided evidence for a unique strategy involved in viral dissemination: HCMV infection of primary human monocytes promotes their transendothelial migration and differentiation into proinflammatory macrophages permissive for the replication of the original input virus. To decipher the mechanism of hematogenous spread, we focused on the viral dysregulation of early cellular processes involved in transendothelial migration. Here, we present evidence that both phosphatidylinositol 3-kinase [PI(3)K] and NF-B activities were crucial for the HCMV induction of monocyte motility and firm adhesion to endothelial cells. We found that the ␤ 1 integrins, the ␤ 2 integrins, intracellular adhesion molecule 1 (ICAM-1), and ICAM-3 were upregulated following HCMV infection and that they played a key role in the firm adhesion of infected monocytes to the endothelium. The viral regulation of adhesion molecule expression is complex, with PI(3)K and NF-B affecting the expression of each adhesion molecule at different stages of the expression cascade. Our data demonstrate key roles for PI(3)K and NF-B signaling in the HCMV-induced cellular changes in monocytes and identify the biological rationale for the activation of these pathways in infected monocytes, which together suggest a mechanism for how HCMV promotes viral spread to and persistence within host organs.

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“…8,9 CLAD was first described in the mid-1970s in Irish Setter dogs in which it was labeled "canine granulocytopathy syndrome." 10 CLAD is characterized by recurrent, life-threatening bacterial infections, which typically lead to death by 6 months of age.…”

Section: Introductionmentioning

confidence: 99%

“…10 CLAD is characterized by recurrent, life-threatening bacterial infections, which typically lead to death by 6 months of age. 9,11 All CLAD dogs are homozygous at the same genetic mutation in the CD18 gene and lack CD18 expression on their leukocytes. 12 We recently established a mixed-breed CLAD colony for the purpose of developing new therapeutic strategies for LAD-I.…”

Section: Introductionmentioning

confidence: 99%