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LC Migration (lc + migration)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

A two-step model for Langerhans cell migration to skin-draining LN

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2008
Eduardo J. Villablanca
Abstract Although the role of Langerhans cells (LC) in skin immune responses is still a matter of debate, it is known that LC require the chemokine receptor CCR7 for migrating to skin-draining LN. A report in the current issue of the European Journal of Immunology unfolds some of the intricacies of LC migration, showing that LC need CXCR4, but not CCR7, for their migration from the epidermis to the dermis. Thus, LC migration to skin-draining LN occurs in two distinct phases: a first step from the epidermis to the dermis regulated by CXCR4 and a second CCR7-dependent step from the dermis to LN. Here we discuss the potential implications of this new two-step LC migration paradigm. [source]

Prominent Langerhans' cell migration in the arthropod bite reactions simulating Langerhans' cell histiocytosis

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 12 2007
Se Hoon Kim
Background:, Epidermal Langerhans' cells (LCs) play pivotal roles in cutaneous immune responses. An encounter with antigens or other stimuli causes the mobilization and migration of LCs. Therefore, some dermatoses, which originated from antigenic stimuli or trauma, can show LC migration. Recently, we experienced several cases of anthropod bites that showed marked inflammatory infiltrates with eosinophils and CD1a-positive LCs. It was difficult to differentiate these cases from Langerhans' cell histiocytosis (LCH). Methods:, The degree and pattern of LC infiltration in the skin of arthropod bite reaction was evaluated. The characteristics of CD1a immunohistochemical expression in the arthropod bite reactions were compared with those of LCH. Results:, A few arthropod bite cases (approximately 36%) showed extensive CD1a-positive LCs in the dermis, especially in the perivascular area. In addition, the CD1a expression patterns of LCs in the arthropod bite reactions were dendritic, whereas that of tumor cells in LCH were distinctly membranous and cytoplasmic. Conclusion:, Some arthropod bite reactions can show marked CD1a-positive LCs in the dermis, especially in the perivascular area. The dendritic CD1a immunohistochemical staining pattern in arthropod bite reactions is useful in helping to differentiate from LCH. [source]

Chronic Ethanol Consumption Decreases Murine Langerhans Cell Numbers and Delays Migration of Langerhans Cells as Well as Dermal Dendritic Cells

ALCOHOLISM, Issue 4 2008
Kristin J. Ness
Background:, Chronic alcoholics experience increased incidence and severity of infections, the mechanism of which is incompletely understood. Dendritic cells (DC) migrate from peripheral locations to lymph nodes (LN) to initiate adaptive immunity against infection. Little is known about how chronic alcohol exposure affects skin DC numbers or migration. Methods:, Mice received 20% EtOH in the drinking water for up to 35 weeks. Baseline Langerhans cell (LC) and dermal DC (dDC) numbers were enumerated by immunofluorescence (IF). LC repopulation after inflammation was determined following congenic bone marrow (BM) transplant and ultraviolet (UV) irradiation. Net LC loss from epidermis was determined by IF following TNF-, or CpG stimulation. LC and dDC migration into LN was assessed by flow cytometry following epicutaneous FITC administration. Results:, Chronic EtOH consumption caused a baseline reduction in LC but not dDC numbers. The deficit was not corrected following transplantation with non-EtOH-exposed BM and UV irradiation, supporting the hypothesis that the defect is intrinsic to the skin environment rather than LC precursors. Net loss of LC from epidermis following inflammation was greatly reduced in EtOH-fed mice versus controls. Ethanol consumption for at least 4 weeks led to delayed LC migration into LN, and consumption for at least 8 weeks led to delayed dDC migration into LN following epicutaneous FITC application. Conclusions:, Chronic EtOH consumption causes decreased density of epidermal LC, which likely results in decreased epidermal immunosurveillance. It also results in altered migratory responsiveness and delayed LC and dDC migration into LN, which likely delays activation of adaptive immunity. Decreased LC density at baseline appears to be the result of an alteration in the skin environment rather than an intrinsic LC defect. These findings provide novel mechanisms to at least partially explain why chronic alcoholics are more susceptible to infections, especially those following skin penetration. [source]

Murine and human Langerhans cells express a functional histamine H4 receptor: modulation of cell migration and function

ALLERGY, Issue 7 2010
M. Gschwandtner
To cite this article: Gschwandtner M, Rossbach K, Dijkstra D, Bäumer W, Kietzmann M, Stark H, Werfel T, Gutzmer R. Murine and human Langerhans cells express a functional histamine H4 receptor: modulation of cell migration and function. Allergy 2010; 65: 840,849. Abstract Background:, Histamine is an important mediator of allergic reactions, and recent studies indicated that the function of different types of antigen presenting cells (APC) can be modulated by histamine, in particular via the newly described histamine H4 receptor (H4R). Therefore, we investigated possible interactions of histamine via the H4R on Langerhans cells (LC), which represent the professional APC in the skin and therefore have an important role in the initiation and maintenance of allergic skin diseases. Methods:, The expression of the H4R was evaluated by real-time PCR, flow cytometry and immunofluorescence staining. The function of the H4R was determined by intracellular flow cytometric measurement of chemokine production and LC migration assays. Results:, Here, we show H4R expression on in vitro generated monocyte-derived LC (mRNA and protein) and on primary LC from murine and human skin samples (protein). The immunofluorescence staining in murine and human skin samples clearly proved that LC express the H4R in situ. Stimulation with histamine or a H4R agonist downregulated the chemokine (C-C motif) ligand 2 (CCL2) in human monocyte-derived LC and primary LC. Prestimulation with a selective H4R antagonist abolished this effect. Moreover, migration of LC from the epidermis was increased after H4R agonist stimulation in ex vivo migration assays using human epidermis and murine in vivo assays. Conclusion:, Our findings show that LC express a functional H4R and point towards a possible pathogenic relevance of the H4R in inflammatory and allergic diseases. [source]