Role of epidermal Langerhans cells in viral infections

1988 ◽  
Vol 103 (1-2) ◽  
pp. 1-14 ◽  
Author(s):  
E. Sprecher ◽  
Y. Becker
Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 579
Author(s):  
Fei Yang ◽  
Lingli Yang ◽  
Lanting Teng ◽  
Huimin Zhang ◽  
Ichiro Katayama

The role of Langerhans cells (LCs) in vitiligo pathogenesis remains unclear, with published studies reporting contradictory results regarding the quantity of LCs and no data on the features of LCs in vitiligo. Here, we aimed to analyze the presence, density, and morphological features of LCs in the epidermis of patients with vitiligo. Skin biopsies were stained for LCs using anti-CD1a/anti-langerin antibodies and analyzed by immunocytochemistry with light and electron microscopy. Compared with healthy controls, we detected significantly increased numbers of epidermal LCs in lesional skin from vitiligo in the progressive state. These LCs exhibited striking morphological alterations, including an elevated number of dendrites, with increased length and more branches than dendrites from controls. Ultrastructure examination via immuno-electron microscopy revealed markedly reduced Birbeck granules (BGs) and shorter BG rods in LCs from progressive vitiligo, with higher expression of langerin. Additionally, expression of S100B, the activity biomarker of vitiligo, was increased in these LCs. This work provides new insight on the cellular composition of LCs in vitiliginous skin, revealing altered morphology and increased LC numbers, with elevated S100B expression. Our data suggest LCs might play a critical role in vitiligo pathogenesis and thus may represent a novel therapeutic target for this disease.


1993 ◽  
Vol 100 (3) ◽  
pp. 282-287 ◽  
Author(s):  
Giampiero Girolomoni ◽  
Maria Lucia Santantonio ◽  
Saveria Pastore ◽  
Paul R. Bergstresser ◽  
Alberto Giannetti ◽  
...  

Parasitology ◽  
2001 ◽  
Vol 123 (4) ◽  
pp. 373-380 ◽  
Author(s):  
M. NARGIS ◽  
M. M. CHISTY ◽  
Y. IHAMA ◽  
H. SATO ◽  
T. INABA ◽  
...  

Several studies have confirmed that epidermal Langerhans' cells (LC) play a central role in the induction of skin-related immunological events. In order to assess the role of LC in Chagas' disease, guinea-pigs were infected intradermally with Trypanosoma cruzi, sacrificed at different time-points, and their tissues were processed for routine histology, electron microscopy and immunohistochemistry. Parasitaemia was observed earliest at day 6 p.i. with 2 peaks at days 9 and 28, and disappeared on day 56 p.i. Parasite-specific serum IgG and IgM were first detected on day 12 p.i. The level of IgG gradually increased by day 84 p.i. All the infected guinea-pigs showed significant alterations in the distribution and morphology of epidermal LC during parasitaemia. The number of LC had significantly decreased in the epidermis by day 3 p.i., only returning to normal levels by day 56 p.i., although the number of LC in the underlying dermis increased concomitantly. Parasites were carried to the regional lymph node, where clustering of parasite-laden dendritic cells (DC) with lymphocytes was seen by electron microscopy. This evidence suggests that LC might be involved in antigen presentation in Chagas' disease.


1992 ◽  
Vol 175 (5) ◽  
pp. 1353-1365 ◽  
Author(s):  
B Wang ◽  
A Rieger ◽  
O Kilgus ◽  
K Ochiai ◽  
D Maurer ◽  
...  

Human epidermal Langerhans cells (LC) bearing IgE are found in disease states associated with hyperimmunoglobulinemia E. When studying the mechanism(s) underlying this phenomenon, immunohistology revealed that a majority of epidermal LC from normal skin of healthy individuals can specifically bind monomeric IgE. IgE binding to LC could neither be prevented by preincubation of the tissue with monoclonal antibodies (mAb) against either Fc epsilon RII/CD23 or Fc gamma RII/CD32, nor by the addition of lactose. However, binding could be entirely abrogated by preincubation with the anti-Fc epsilon RI alpha mAb 15-1, which interferes with IgE binding to Fc epsilon RI alpha gamma transfectants. These observations indicated that IgE binding to epidermal LC is mediated by Fc epsilon RI rather than by CD23, CD32, or the D-galactose-specific IgE-binding protein. This assumption gained support from our additional findings that: (a) the majority of LC exhibited distinct surface immunolabeling with the anti-Fc epsilon RI alpha mAbs 15-1 and 19-1, but not with any of eight different anti-Fc epsilon RII/CD23 mAbs; and (b) transcripts for the alpha, beta, and gamma chains of Fc epsilon RI could be amplified by polymerase chain reaction from RNA preparations of LC-enriched, but not of LC-depleted, epidermal cell suspensions. In view of the preeminent role of Fc epsilon RI crosslinking on mast cells and basophils in triggering the synthesis and release of mediators of allergic reactions, the demonstration of this receptor on epidermal LC may have important implications for our understanding of allergic reactions after epicutaneous contact with allergens.


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