Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.712676
Keywords
atopic dermatitis; dendritic cells; type 2 immune responses; immune homeostasis; homeostatic feedback loop
Categories
Funding
- Ministry of Education, Science and Culture of Japan [18H02670, 16K15291, 17K15027, 17K15732, 18K15194]
- Project for Cancer Research And Therapeutic Evolution (P-CREATE) from Japan Agency for Medical Research and development (AMED) [16cm0106307h0001, 17cm0106307h0002, 18cm0106307h0003, 19cm0106307h0004]
- Uehara Memorial Foundation
- Takeda Science Foundation
- Naito Foundation
- Bristol-Myers Squibb Foundation
- GSK Japan
- Daiichi Sankyo Foundation of Life Science
- Nipponham Foundation for the Future of Food
- Shin-Nihon Foundation of Advanced Medical Research
- Nazarbayev University Faculty Development Grant [090118FD5310]
- Grants-in-Aid for Scientific Research [17K15732, 16K15291, 17K15027, 18H02670, 18K15194] Funding Source: KAKEN
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Atopic dermatitis is a common inflammatory skin disease characterized by immune abnormalities and impaired skin barrier function. The research indicates that the absence of cDCs may exacerbate immune abnormalities, accelerate the colonization of Staphylococcus aureus on the skin, and worsen the symptoms of the disease.
Atopic dermatitis (AD) is a common pruritic inflammatory skin disease characterized by impaired epidermal barrier function and dysregulation of Thelper-2 (T(H)2)-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 CD11c(hi) 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.
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