Association of basal-lamina defects with epidermal and dermal T6-positive cells: Evidence of Langerhans-cell migration

1985 ◽  
Vol 278 (2) ◽  
pp. 126-132 ◽  
Author(s):  
G. F. Murphy ◽  
E. Fonferko ◽  
T. Flotte ◽  
A. K. Bhan
Keyword(s):  
Cell Migration ◽  
Basal Lamina ◽  
Langerhans Cell

Guttate psoriasis is associated with an intermediate phenotype of impaired Langerhans cell migration

2014 ◽  
Vol 171 (2) ◽  
pp. 409-411 ◽  
Author(s):  
L.H. Eaton ◽  
L. Chularojanamontri ◽  
F.R. Ali ◽  
E. Theodorakopoulou ◽  
R.J. Dearman ◽  
...  
Keyword(s):  
Cell Migration ◽  
Langerhans Cell ◽  
Intermediate Phenotype ◽  
Guttate Psoriasis

Skin irritants and contact sensitizers induce Langerhans cell migration and maturation at irritant concentration

2006 ◽  
Vol 15 (6) ◽  
pp. 432-440 ◽  
Author(s):  
John J. L. Jacobs ◽  
Cynthia L. Lehe ◽  
Hitoshi Hasegawa ◽  
Graham R. Elliott ◽  
Pranab K. Das
Keyword(s):  
Cell Migration ◽  
Langerhans Cell ◽  
Skin Irritants

Conjunctival inflammation induces langerhans cell migration into the cornea

2000 ◽  
Vol 21 (1) ◽  
pp. 550-553 ◽  
Author(s):  
Tomo Suzuki ◽  
Yoichiro Sano ◽  
Shigeru Kinoshita
Keyword(s):  
Cell Migration ◽  
Langerhans Cell ◽  
Conjunctival Inflammation

scholarly journals EC-SOD Suppresses Contact Hypersensitivity in Mouse Skin by Impairing Langerhans Cell Migration

2007 ◽  
Vol 127 (8) ◽  
pp. 1930-1937 ◽  
Author(s):  
Kwangmin Na ◽  
Kyoung-Eun Kim ◽  
Sang-Tae Park ◽  
Tae-Yoon Kim
Keyword(s):  
Cell Migration ◽  
Mouse Skin ◽  
Langerhans Cell ◽  
Contact Hypersensitivity

Exogenous topical lactoferrin inhibits allergen-induced Langerhans cell migration and cutaneous inflammation in humans

2001 ◽  
Vol 144 (4) ◽  
pp. 715-725 ◽  
Author(s):  
C.E.M. Griffiths ◽  
M. Cumberbatch ◽  
S.C. Tucker ◽  
R.J. Dearman ◽  
S. Andrew ◽  
...  
Keyword(s):  
Cell Migration ◽  
Langerhans Cell ◽  
Cutaneous Inflammation

scholarly journals Evidence for a novel enzymatic mechanism of neural crest cell migration on extracellular glycoconjugate matrices.

1986 ◽  
Vol 102 (2) ◽  
pp. 432-441 ◽  
Author(s):  
R B Runyan ◽  
G D Maxwell ◽  
B D Shur
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Neural Crest ◽  
Basal Lamina ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Crest Cell Migration ◽  
Dose Dependent ◽  
Crest Cell

Migrating embryonic cells have high levels of cell surface galactosyltransferase (GalTase) activity. It has been proposed that GalTase participates during migration by recognizing and binding to terminal N-acetylglucosamine (GlcNAc) residues on glycoconjugates within the extracellular matrix (Shur, B. D., 1982, Dev. Biol. 91:149-162). We tested this hypothesis using migrating neural crest cells as an in vitro model system. Cell surface GalTase activity was perturbed using three independent sets of reagents, and the effects on cell migration were analyzed by time-lapse microphotography. The GalTase modifier protein, alpha-lactalbumin (alpha-LA), was used to inhibit surface GalTase binding to terminal GlcNAc residues in the underlying substrate. alpha-LA inhibited neural crest cell migration on basal lamina-like matrices in a dose-dependent manner, while under identical conditions, alpha-LA had no effect on cell migration on fibronectin. Control proteins, such as lysozyme (structurally homologous to alpha-LA) and bovine serum albumin, did not effect migration on either matrix. Second, the addition of competitive GalTase substrates significantly inhibited neural crest cell migration on basal lamina-like matrices, but as above, had no effect on migration on fibronectin. Comparable concentrations of inappropriate sugars also had no effect on cell migration. Third, addition of the GalTase catalytic substrate, UDPgalactose, produced a dose-dependent increase in the rate of cell migration. Under identical conditions, the inappropriate sugar nucleotide, UDPglucose, had no effect. Quantitative enzyme assays confirmed the presence of GalTase substrates in basal lamina matrices, their absence in fibronectin matrices, and the ability of alpha-LA to inhibit GalTase activity towards basal lamina substrates. Laminin was found to be a principle GalTase substrate in the basal lamina, and when tested in vitro, alpha-LA inhibited cell migration on laminin. Together, these experiments show that neural crest cells have at least two distinct mechanisms for interacting with the substrate during migration, one that is fibronectin-dependent and one that uses GalTase recognition of basal lamina glycoconjugates.

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