Monocyte-derived dendritic cells from patients with dermatophytosis restrict the growth of Trichophyton rubrum and induce CD4-T cell activation
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Updated: Apr 21, 2026
Generation of Human Monocyte-derived Dendritic Cells from Whole Blood
Published on: December 24, 2016
Karla Santiago1, Gisele Facholi Bomfim1, Paulo Ricardo Criado2
1Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, Brazil.
Abstract:
Dermatophytes are the most common agents of superficial mycoses that are caused by mold fungi. Trichophyton rubrum is the most common pathogen causing dermatophytosis. The immunology of dermatophytosis is currently poorly understood. Recently, our group investigated the interaction of T. rubrum conidia with peritoneal mouse macrophages. We found that macrophages phagocytose T. rubrum conidia resulted in a down-modulation of class II major histocompatibility complex (MHC) antigens and in the expression of co-stimulatory molecules. Furthermore, it induced the production of IL-10, and T. rubrum conidia differentiated into hyphae that grew and killed the macrophages after 8 hrs of culture. This work demonstrated that dendritic cells (DCs) and macrophages, from patients or normal individuals, avidly interact with pathogenic fungus T. rubrum. The dermatophyte has two major receptors on human monocyte-derived DC: DC-SIGN and mannose receptor. In contrast macrophage has only mannose receptor that participates in the phagocytosis or bound process. Another striking aspect of this study is that unlike macrophages that permit rapid growth of T. rubrum, human DC inhibited the growth and induces Th activation. The ability of DC from patients to interact and kill T. rubrum and to present Ags to T cells suggests that DC may play an important role in the host response to T. rubrum infection by coordinating the development of cellular immune response.
Insights
This study reveals how Trichophyton rubrum interacts with immune cells. Macrophages are killed by the fungus, while dendritic cells (DCs) control its growth and activate T cells, highlighting DCs' crucial role in fighting dermatophytosis.
Area of Science:
- Immunology
- Mycology
- Dermatology
Background:
- Dermatophytes, like Trichophyton rubrum, are common causes of superficial fungal infections (mycoses).
- The immune response to dermatophytosis, particularly the role of macrophages and dendritic cells (DCs), is not well understood.
- T. rubrum is the most prevalent fungal pathogen responsible for dermatophytosis.
Purpose of the Study:
- To investigate the interaction between T. rubrum conidia and host immune cells, specifically macrophages and dendritic cells (DCs).
- To elucidate the immunological mechanisms underlying the host's response to T. rubrum infection.
Main Methods:
- Co-culture of T. rubrum conidia with mouse peritoneal macrophages and human monocyte-derived dendritic cells (DCs).
- Analysis of macrophage and DC surface marker expression, including MHC class II and co-stimulatory molecules.
- Assessment of cytokine production (e.g., IL-10) and fungal growth within immune cells.
- Evaluation of T. rubrum's effect on macrophage viability and DC-mediated T cell activation.
Main Results:
- Macrophages phagocytosed T. rubrum conidia, leading to down-modulation of MHC class II and co-stimulatory molecules, IL-10 production, and subsequent fungal hyphal growth and macrophage death.
- Human monocyte-derived DCs efficiently interacted with T. rubrum via DC-SIGN and mannose receptors.
- Unlike macrophages, DCs inhibited T. rubrum growth and induced T helper (Th) cell activation.
- DCs from patients demonstrated an ability to interact with, kill T. rubrum, and present antigens to T cells.
Conclusions:
- Macrophages are susceptible to T. rubrum, exhibiting impaired immune signaling and succumbing to fungal growth.
- Dendritic cells (DCs) play a critical role in controlling T. rubrum infection by inhibiting fungal growth and initiating adaptive cellular immunity.
- DCs are key orchestrators of the host immune response to T. rubrum, coordinating anti-fungal immunity through antigen presentation and Th activation.
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