Langerhans Cells Require MyD88-Dependent Signals for Candida albicans Response but Not for Contact Hypersensitivity or Migration
Open accessAbstract
Langerhans cells (LC) are a subset of skin-resident dendritic cells (DC) that reside in the epidermis as immature DC, where they acquire Ag. A key step in the life cycle of LC is their activation into mature DC in response to various stimuli, including epicutaneous sensitization with hapten and skin infection with Candida albicans. Mature LC migrate to the skin-draining LN, where they present Ag to CD4 T cells and modulate the adaptive immune response. LC migration is thought to require the direct action of IL-1β and IL-18 on LC. In addition, TLR ligands are present in C. albicans, and hapten sensitization produces endogenous TLR ligands. Both could contribute to LC activation. We generated Langerin-Cre MyD88fl mice in which LC are insensitive to IL-1 family members and most TLR ligands. LC migration in the steady state, after hapten sensitization and postinfection with C. albicans, was unaffected. Contact hypersensitivity in Langerin-Cre MyD88fl mice was similarly unaffected. Interestingly, in response to C. albicans infection, these mice displayed reduced proliferation of Ag-specific CD4 T cells and defective Th17 subset differentiation. Surface expression of costimulatory molecules was intact on LC, but expression of IL-1β, IL-6, and IL-23 was reduced. Thus, sensitivity to MyD88-dependent signals is not required for LC migration, but is required for the full activation and function of LC in the setting of fungal infection.
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Upon antigen encounter and recognition via TLRs and C-lectin receptors, Langerhans cells become activated and migrate to cutaneous lymph nodes to prime naïve lymphocytes.
“Upon antigen encounter and recognition via TLRs and C-lectin receptors (CLRs), LCs become activated and migrate to cutaneous lymph nodes to prime naïve lymphocytes [33].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [33]
The Introduction (page not provided) says Langerhans cells acquire antigen in skin, migrate to cutaneous lymph nodes, and present it to T cells; it also describes peripheral dendritic cells presenting antigen to naïve T cells. But the Discussion says direct MyD88-dependent TLR signaling is not required for Langerhans-cell migration after the stimuli tested, and our copy does not establish CLR recognition as the trigger for the claimed sequence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredConsuming a high-fat diet alters skin architecture and local immune responses.
“Consuming a high-fat diet has been shown to alter skin architecture and local immune responses [33]”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [33]
The Results and Discussion address skin immune responses to Candida albicans infection and contact sensitization, not high-fat-diet consumption. A References entry mentions diet-induced obesity in a study of CNS signaling, but our copy does not report that a high-fat diet alters skin architecture or local immune responses (searched: high-fat diet, skin architecture, and diet-induced obesity). (LLM, conf=0.76)
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Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection
Cardozo, M. E., Cirilo, T. M., Duval, I. D. B., de Oliveira, A. L. G., Magalhães, L. M. D., Bueno, L. L., Dumonteil, E., & Fujiwara, R. T. (2026) · Clinical Reviews in Allergy & Immunology · doi:10.1007/s12016-026-09195-x
- Authors
- Haley, K., Igyártó, B. Z., Ortner, D., Bobr, A., Kashem, S., Schenten, D., & Kaplan, D. H.
- Affiliations
- University of Minnesota (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Haley, Krystal
- Ortner, Daniela
- Bobr, Aleh
- Kashem, Sakeen
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-05-01
- Volume
- 188
- Issue
- 9
- Pages
- 4334-4339
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3331889
- OpenAlex
- W1915611502
- Cited by
- 61
- References
- 31
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 6 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 7 · 2015: 5 · 2014: 9 · 2013: 8 · 2012: 5
- FWCI
- 3.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Cancer Research Institute
- Dermatology Foundation (AR056632)
- American Skin Association (AR056632)
- University of Minnesota
- National Institutes of Health (5r01ar056632-05, AR056632)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR060744, AR060744, AR056632, R01-AR056632)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- Langerhans cells, MyD88, Candida albicans, contact hypersensitivity, dendritic cell migration, dendritic cell activation, IL-1β, IL-18, Toll-like receptor signaling, Th17 cell differentiation, CD4+ T cell proliferation, IL-23, interleukin-6, skin-draining lymph nodes, fungal skin infection, hapten sensitization
- MeSH terms
- Animals, Antigens, Fungal, Candida albicans, Candidiasis, Cell Movement, Dermatitis, Contact, Dermatomycoses, Haptens, Interleukins, Langerhans Cells, Lymphocyte Activation, Signal Transduction, Mice, Knockout, Mice, Myeloid Differentiation Factor 88, Th17 Cells
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