Phenotyping of epidermal dendritic cells allows the differentiation between extrinsic and intrinsic forms of atopic dermatitis

2000 ◽  
Vol 143 (6) ◽  
pp. 1193-1198 ◽  
Author(s):  
T. Oppel ◽  
E. Schuller ◽  
S. Günther ◽  
M. Moderer ◽  
J. Haberstok ◽  
...  
2017 ◽  
Vol 56 (6) ◽  
pp. 630-635 ◽  
Author(s):  
Vanessa G. dos Santos ◽  
Raquel L. Orfali ◽  
Tiago de Oliveira Titz ◽  
Alberto J. da Silva Duarte ◽  
Maria N. Sato ◽  
...  

2021 ◽  
Vol 8 (3) ◽  
pp. 426-441
Author(s):  
Ryoji Tanei ◽  
Yasuko Hasegawa

The immunopathogenic role of house dust mite (HDM) allergens in the development of skin lesions in atopic dermatitis (AD) has not yet been precisely clarified. We immunohistopathologically evaluated the localization of immunoglobulin E (IgE)-positive epidermal dendritic cells with HDM antigens in the skin lesions of patients with IgE-allergic AD. Using double-immunofluorescence and single-immunochemical staining methods, we analyzed biopsy specimens from the skin lesions of six patients with IgE-allergic AD and HDM allergy and 11 control subjects with inflammatory skin disorders. Inflammatory dendritic epidermal cells (IDECs; CD11c+ and CD206+ cells) were markedly observed in the central area of the spongiotic epidermis of skin lesions in all AD patients. Furthermore, IgE-positive IDECs with HDM antigens in the central areas of the spongiosis were found in four of the six (66.7%) AD patients. Langerhans cells (LCs; CD207+ cells) with HDM antigens were also observed in the peripheral areas of the spongiosis. Infiltration of CD4+ and CD8+ T cells in association with IgE-positive IDECs and LCs with HDM antigens was seen in the spongiotic epidermis. An IgE-mediated delayed-type hypersensitivity reaction, in combination with IgE-bearing dendritic cells, specific T cells, keratinocytes, and HDM antigens, may lead to spongiotic tissue formation in eczematous dermatitis in AD.


1999 ◽  
Vol 4 (2) ◽  
pp. 169-172 ◽  
Author(s):  
Koichiro Nakamura ◽  
Kunihiko Tamaki ◽  
Atsushi Saitoh ◽  
Nami Yasaka ◽  
Masutaka Furue

1998 ◽  
Vol 187 (10) ◽  
pp. 1623-1631 ◽  
Author(s):  
Jeanette C. Reece ◽  
Amanda J. Handley ◽  
E. John Anstee ◽  
Wayne A. Morrison ◽  
Suzanne M. Crowe ◽  
...  

Macrophage tropic HIV-1 is predominant during the initial viremia after person to person transmission of HIV-1 (Zhu, T., H. Mo, N. Wang, D.S. Nam, Y. Cao, R.A. Koup, and D.D. Ho. 1993. Science. 261:1179–1181.), and this selection may occur during virus entry and carriage to the lymphoid tissue. Human skin explants were used to model HIV-1 selection that may occur at the skin or mucosal surface. Macrophage tropic, but not T cell line tropic strains of HIV-1 applied to the abraded epidermis were recovered from the cells emigrating from the skin explants. Dermis and epidermis were separated by dispase digestion after virus exposure to determine the site of viral selection within the skin. Uptake and transmission to T cells of all HIV-1 isolates was found with the dermal emigrant cells, but only macrophage tropic virus was transferred by emigrants from the epidermis exposed to HIV-1, indicating selection only within the epidermis. CD3+, CD4+ T cells were found in both the dermal and epidermal emigrant cells. After cell sorting to exclude contaminating T cells, macrophage tropic HIV-1 was found in both the dermal emigrant dendritic cells and in dendritic cells sorted from the epidermal emigrants. These observations suggest that selective infection of the immature epidermal dendritic cells represents the cellular mechanism that limits the initial viremia to HIV-1 that can use the CCR5 coreceptor.


1987 ◽  
Vol 42 (3) ◽  
pp. 328-337 ◽  
Author(s):  
Donald Y.M. Leung ◽  
Eveline E. Schneeberger ◽  
Reuben P. Siraganian ◽  
Raif S. Geha ◽  
Atul K. Bhan

2015 ◽  
Vol 7 (3) ◽  
Author(s):  
Fernanda Berti Rocha Mendes ◽  
Raquel de Paula Ramos Castro ◽  
Mariana Petaccia de Macedo ◽  
Clovis Antonio Lopes Pinto ◽  
João Pedreira Duprat Neto ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Yotaro Nishikawa ◽  
Tomohiro Fukaya ◽  
Takehito Fukui ◽  
Tomofumi Uto ◽  
Hideaki Takagi ◽  
...  

Atopic dermatitis (AD) is a common pruritic inflammatory skin disease characterized by impaired epidermal barrier function and dysregulation of Thelper-2 (TH2)-biased immune responses. While the lineage of conventional dendritic cells (cDCs) are implicated to play decisive roles in T-cell immune responses, their requirement for the development of AD remains elusive. Here, we describe the impact of the constitutive loss of cDCs on the progression of AD-like inflammation by using binary transgenic (Tg) mice that constitutively lacked CD11chi cDCs. Unexpectedly, the congenital deficiency of cDCs not only exacerbates the pathogenesis of AD-like inflammation but also elicits immune abnormalities with the increased composition and function of granulocytes and group 2 innate lymphoid cells (ILC2) as well as B cells possibly mediated through the breakdown of the Fms-related tyrosine kinase 3 ligand (Flt3L)-mediated homeostatic feedback loop. Furthermore, the constitutive loss of cDCs accelerates skin colonization of Staphylococcus aureus (S. aureus), that associated with disease flare. Thus, cDCs maintains immune homeostasis to prevent the occurrence of immune abnormalities to maintain the functional skin barrier for mitigating AD flare.


Sign in / Sign up

Export Citation Format

Share Document