Abstract

The C-type lectin receptor Dectin-1 was originally described as the β-glucan receptor expressed in myeloid cells, with crucial functions in antifungal responses. However, over time, different ligands both of microbial-derived and endogenous origin have been shown to be recognized by Dectin-1. The outcomes of this recognition are diverse, including pro-inflammatory responses such as cytokine production, reactive oxygen species generation and phagocytosis. Nonetheless, tolerant responses have been also attributed to Dectin-1, depending on the specific ligand engaged. Dectin-1 recognition of their ligands triggers a plethora of downstream signaling pathways, with complex interrelationships. These signaling routes can be modulated by diverse factors such as phosphatases or tetraspanins, resulting either in pro-inflammatory or regulatory responses. Since its first depiction, Dectin-1 has recently gained a renewed attention due to its role in the induction of trained immunity. This process of long-term memory of innate immune cells can be triggered by β-glucans, and Dectin-1 is crucial for its initiation. The main signaling pathways involved in this process have been described, although the understanding of the above-mentioned complexity in the β-glucan-induced trained immunity is still scarce. In here, we have reviewed and updated all these factors related to the biology of Dectin-1, highlighting the gaps that deserve further research. We believe on the relevance to fully understand how this receptor works, and therefore, how we could harness it in different pathological conditions as diverse as fungal infections, autoimmunity, or cancer.

Highlights

  • The vertebrate immune system is characterized by both an early innate and an adaptive immunity

  • We aim to compile and update the current knowledge on the C-type Lectin Receptors (CLRs) DEndritic cell-associated C-type lecTIN receptor-1, Dectin-1, its expression pattern, ligands, and the signaling pathways ignited downstream its activation. This receptor is a key component of the revolutionizing concept of trained immunity (TI), a process of long-term memory developed by innate immune cells

  • This topic deserves to be studied in detail, as decoding the mechanisms implicated in Dectin-1-triggered IFN-I production would provide new potential tools against the clinically relevant systemic Candida albicans infection, with up to 40% of mortality rate in intensive care units services [109]

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Summary

Frontiers in Immunology

Over time, different ligands both of microbial-derived and endogenous origin have been shown to be recognized by Dectin-1 The outcomes of this recognition are diverse, including proinflammatory responses such as cytokine production, reactive oxygen species generation and phagocytosis. Dectin-1 recognition of their ligands triggers a plethora of downstream signaling pathways, with complex interrelationships. These signaling routes can be modulated by diverse factors such as phosphatases or tetraspanins, resulting either in pro-inflammatory or regulatory responses. Dectin-1 has recently gained a renewed attention due to its role in the induction of trained immunity This process of long-term memory of innate immune cells can be triggered by b-glucans, and Dectin-1 is crucial for its initiation.

INTRODUCTION
Microbial PAMPs
Dendritic cells Macrophages
Modulating Signaling Pathways
TRAINED IMMUNITY
Findings
OPEN QUESTIONS
Full Text
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