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PubMed2024

The Dectin-1 and Dectin-2 clusters: C-type lectin receptors with fundamental roles in immunity.

The ability of myeloid cells to recognize and differentiate endogenous or exogenous ligands rely on the presence of different transmembrane protein receptors. C-type lectin receptors (CLRs), defined by the presence of a conserved structural motif called C-type lectin-like domain (CTLD), are a crucial family of receptors involved in this process, being able to recognize a diverse range of ligands from glycans to proteins or lipids and capable of initiating an immune response. The Dectin-1 and Dectin-2 clusters involve two groups of CLRs, with genes genomically linked within the natural killer cluster of genes in both humans and mice, and all characterized by the presence of a single extracellular CTLD. Fundamental immune cell functions such as antimicrobial effector mechanisms as well as internalization and presentation of antigens are induced and/or regulated through activatory, or inhibitory signalling pathways triggered by these receptors after ligand binding. In this review, we will discuss the most recent concepts regarding expression, ligands, signaling pathways and functions of each member of the Dectin clusters of CLRs, highlighting the importance and diversity of their functions.

Lectins, C-Type↗
PubMed2026

Profiling Dectin-2-Positive Tumor-Associated Macrophages Across Human Cancers by Immunohistochemistry.

PURPOSE: To characterize the prevalence and distribution of Dectin-2-positive macrophages across human tumors and develop a research immunohistochemistry (IHC) assay to assess Dectin-2 in cancer tissues. MATERIALS AND METHODS: C-type lectin domain family 6 member A (CLEC6A), the gene encoding Dectin-2, was evaluated across 38 tumor types using The Cancer Genome Atlas. A fit-for-purpose Dectin-2 IHC assay was developed using a monoclonal antibody selected from screening 11 anti-Dectin-2 antibodies. Assay performance was supported by Dectin-2-expressing and parental cell line controls, macrophage-associated staining patterns, and comparison with an orthogonal CLEC6A in situ hybridization method using RNAscope. Dectin-2 expression was assessed in tissue microarrays (n = 553 samples) across 6 cancer types and whole tissue sections (n = 137) across 7 cancer types. RESULTS: The Cancer Genome Atlas analysis identified enriched CLEC6A expression in several tumor types, including non-small cell lung cancer (NSCLC), triple-negative breast cancer (TNBC), and subsets of head and neck cancer (HNC) and colorectal cancer (CRC). By IHC, Dectin-2-positive macrophages were detected across tumor types, with notable heterogeneity within and across cancer types. In tissue microarrays, NSCLC showed the highest frequency of Dectin-2-positive macrophage infiltration, with 38% of cases with staining ≥1% of tumor area. Whole tissue section analysis confirmed and expanded these findings, with ≥50% of NSCLC, melanoma, HNC, TNBC, and CRC samples showing Dectin-2-positive macrophages in ≥1% tumor area. CONCLUSIONS: Dectin-2 expression was observed in subsets of tumor-associated macrophages across multiple human cancers, with relatively enriched expression in NSCLC, melanoma, HNC, TNBC, and CRC. To our knowledge, this study represents the first broad protein-level characterization of Dectin-2 across multiple human tumor types, identifies cancers with relatively enriched Dectin-2-positive macrophage infiltration, and provides a foundation for future translational studies of Dectin-2-targeted therapies.

Humans↗
PubMed2025

TNF-α/NF-κB mediated upregulation of Dectin-1 in hyperglycemic obesity: implications for metabolic inflammation and diabetes.

BACKGROUND: Dectin-1, a key innate immune receptor, plays a critical role in cellular responses and is implicated in chronic inflammation and metabolic syndromes. This study addresses a pivotal gap in elucidating the regulatory mechanism governing Dectin-1 expressionin obesity and diabetes, hypothesizing that hyperglycemia and TNF-&#x3b1; synergistically upregulate Dectin-1 in adipose tissue (AT), thereby exacerbating inflammatory responses and contributing to metabolic dysfunction. METHODS: The study included 95 overweight and obese Kuwaiti individuals, categorized into prediabetic (HbA1c&#x2009;<&#x2009;6.5%) and diabetic (HbA1c&#x2009;&#x2265;&#x2009;6.5%) groups. Anthropometric and clinical measurements were recorded. AT biopsies were obtained for RNA extraction and immunohistochemistry. Pre-adipocytes from lean and obese individuals were cultured, differentiated into adipocytes, and treated with TNF-&#x3b1; under normal or high-glucose conditions to assess Dectin-1 expression. Chromatin immunoprecipitation (ChIP) assays analyzed NF-&#x3ba;B binding to the Dectin-1 promoter. Wildtype and TNF-&#x3b1;-/- mice were used to evaluate TNF-&#x3b1;'s effect on Dectin-1 expression in AT. RESULTS: Our data demonstrate that hyperglycemic obesity significantly induces Dectin-1 expression in AT through the TNF-&#x3b1;/NF-&#x3ba;B signaling pathway. In a cohort of 95 obese individuals, subdivided into prediabetics (HbA1c&#x2009;<&#x2009;6.5%, n&#x2009;=&#x2009;49) and diabetics (HbA1c&#x2009;&#x2265;&#x2009;6.5%, n&#x2009;=&#x2009;46), a strong positive correlation was observed between AT Dectin-1 transcripts and plasma HbA1c levels exclusively in diabetic participants, underscoring the specificity of Dectin-1 upregulation in hyperglycemic conditions. Elevated Dectin-1 expression was consistently associated to increased inflammation markers. Immunohistochemical analysis revealed co-localization and concurrent upregulation of Dectin-1 and TNF-&#x3b1; proteins in hyperglycemic AT. Functional assays in TNF-&#x3b1; deficient mice and human adipocytes further validated that TNF-&#x3b1; and hyperglycemia act cooperatively to regulate Dectin-1 expression. Mechanistically, we demonstrated that NF-&#x3ba;B directly binds to the Dectin-1 promoter, mediating its transcriptional activation in response to glucose and TNF-&#x3b1;. CONCLUSION: This study significantly advances the understanding of upregulation Dectin-1 in metabolic inflammation, filling a crucial niche in diabetes research and suggesting new therapeutic targets for obesity-related metabolic disorders.

Humans↗