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Last update 08 May 2025

CLEC4K

Last update 08 May 2025

Basic Info

Synonyms

C-type lectin domain family 4 member K, CD207, CD207 molecule

+ [2]

Introduction

Calcium-dependent lectin displaying mannose-binding specificity. Induces the formation of Birbeck granules (BGs); is a potent regulator of membrane superimposition and zippering. Binds to sulfated as well as mannosylated glycans, keratan sulfate (KS) and beta-glucans. Facilitates uptake of antigens and is involved in the routing and/or processing of antigen for presentation to T cells. Major receptor on primary Langerhans cells for Candida species, Saccharomyces species, and Malassezia furfur. Protects against human immunodeficiency virus-1 (HIV-1) infection. Binds to high-mannose structures present on the envelope glycoprotein which is followed by subsequent targeting of the virus to the Birbeck granules leading to its rapid degradation.

Drugs associated with CLEC4K

CD207 CAR-T cells(Beijing Friendship Hospital)

Target

CLEC4K

Mechanism

CLEC4K inhibitors [+1]

Active Org.

Beijing Friendship Hospital

Originator Org.-

Active Indication

Refractory Langerhans Cell Histiocytosis

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2024079352

Patent Mining

Target

CLEC4K

Mechanism-

Active Org.

Cutanos GmbH

Originator Org.

Cutanos GmbH

Active Indication

Immune System Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CLEC4K

NCT05477446

/ Not yet recruitingPhase 1IIT

Safety and Efficacy of CD207 Targeted CAR-T Cell Therapy in Patients With Relapsed and Refractory (R/R) Langerhans Cell Histiocytosis

This is a single-arm study to evaluate the efficacy and safety of CD207 targeted CAR-T cell therapy in relapsed and refractory langerhans cell histiocytosis.

Start Date01 Oct 2022

Sponsor / Collaborator

Beijing Friendship Hospital

[+1]

100 Clinical Results associated with CLEC4K

100 Translational Medicine associated with CLEC4K

0 Patents (Medical) associated with CLEC4K

1,034

Literatures (Medical) associated with CLEC4K

01 Apr 2025·Experimental Dermatology

Early Neutrophil Activation in Psoriatic Skin at Relapse Following Dead Sea Climatotherapy

Article

Author: Steiniche, Torben ; Johansen, Claus ; Bregnhøj, Anne ; Emmanuel, Thomas ; Rather, Ida Maja ; Ben Abdallah, Hakim ; Iversen, Lars ; Baez, Elena

ABSTRACTPsoriasis, a chronic inflammatory skin disorder characterised by erythematous and scaly plaques, can be both physically and emotionally distressing for patients. Dead Sea climatotherapy (DSC), a treatment modality combining sun exposure, mineral‐rich water and mud therapy during 4 weeks at Ein Gedi, Israel, is used for a small group of patients with psoriasis. This study aimed to investigate the cellular composition of psoriatic skin lesions at relapse after complete clearance from DSC. Skin biopsies from baseline, end of treatment and relapse were collected from eight patients with plaque psoriasis who achieved complete clearance from Dead Sea climatotherapy treatment. These biopsies were subjected to immunohistochemistry, RNA sequencing and quantitative polymerase chain reaction analysis (qPCR). Our findings demonstrate that DSC effectively reduces inflammatory markers to levels comparable to baseline non‐lesional skin in the short term. The differential expression analysis identified several upregulated differentially expressed genes, including OSM, CXCL8, TREM1, CXCL1, CSF3R, BCL2A1 and CXCL2, in relapsed psoriasis skin compared with baseline lesional skin. These findings were confirmed by qPCR analysis. Pathway enrichment analysis indicated a marked upregulation of neutrophil‐associated pathways in relapse skin compared with baseline lesional skin. Immunohistochemical staining for neutrophil markers, such as CD11b, CD15, CD66b, CD207, MPO and NE, showed a non‐significant trend towards enhanced neutrophil infiltration and activation at relapse. In conclusion, while DSC provides short‐term effectiveness in managing psoriasis, the initial relapse phase is associated with neutrophil activation and migration. Thus, targeting neutrophils early in the psoriasis disease course may disturb the evolution of psoriasis, potentially preventing disease chronicity.

20 Feb 2025·Blood

BRAFV600E induces key features of LCH in iPSCs with cell type–specific phenotypes and drug responses

Article

Author: Hafemeister, Christoph ; Halbritter, Florian ; Simonitsch-Klupp, Ingrid ; Abagnale, Giulio ; Hutter, Caroline ; Distel, Martin ; Rados, Magdalena ; van Midden, Wouter ; Pötschger, Ulrike ; Schwentner, Raphaela ; Sturtzel, Caterina ; Eder, Sebastian K. ; Taschner-Mandl, Sabine ; Ben Soussia-Weiss, Philipp

AbstractLangerhans cell histiocytosis (LCH) is a clonal hematopoietic disorder defined by tumorous lesions containing CD1a+/CD207+ cells. Two severe complications of LCH are systemic hyperinflammation and progressive neurodegeneration. The scarcity of primary samples and lack of appropriate models limit our mechanistic understanding of LCH pathogenesis and affect patient care. We generated a human in vitro model for LCH using induced pluripotent stem cells (iPSCs) harboring the BRAFV600E mutation, the most common genetic driver of LCH. We show that BRAFV600E/WT iPSCs display myelomonocytic skewing during hematopoiesis and spontaneously differentiate into CD1a+/CD207+ cells that are similar to lesional LCH cells and are derived from a CD14+ progenitor. We show that BRAFV600E modulates the expression of key transcription factors regulating monocytic differentiation and leads to an upregulation of proinflammatory molecules and LCH marker genes early during myeloid differentiation. In vitro drug testing revealed that BRAFV600E-induced transcriptomic changes are reverted upon treatment with mitogen-activated protein kinase (MAPK) pathway inhibitors (MAPKis). Importantly, MAPKis do not affect myeloid progenitors but reduce only the mature CD14+ cell population. Furthermore, iPSC-derived neurons (iNeurons) cocultured with BRAFV600E/WT iPSC-derived microglia-like cells, differentiated from iPSC-derived CD34+ progenitors, exhibit signs of neurodegeneration with neuronal damage and release of neurofilament light chain. In summary, the iPSC-based model described here provides a platform to investigate the effects of BRAFV600E in different hematopoietic cell types and provides a tool to compare and identify novel approaches for the treatment of BRAFV600E-driven diseases.

01 Feb 2025·The Journal of Dermatology

A case of indeterminate cell histiocytosis with ETV3‐NCOA2 translocation

Article

Author: Baba, Satoshi ; Tajima, Mizuho ; Nagakura, Yuka ; Ajima, Sayaka ; Kageyama, Reiko ; Shimauchi, Takatoshi ; Kitauchi, Yurie ; Suzuki, Norihito ; Takahashi, Juri ; Honda, Tetsuya

AbstractIndeterminate cell histiocytosis (ICH) is a rare histiocytic disorder characterized by a proliferation of CD1a+ and CD207/langerin− cells. Recent molecular analyses have identified ETV3‐NCOA2 translocation as a possible aetiopathogenesis of ICH. Herein, we describe the first Japanese case of ICH with ETV3‐NCOA2 translocation. A 79‐year‐old Japanese man presented with a 1‐year history of pruritic erythematous papules and nodules on his trunk and extremities. Histological examination revealed a dense and diffuse sheets–like infiltration of medium‐sized histiocyte‐like cells from the epidermis to the deep dermis. Immunohistochemically, the atypical cells were positive for CD1a but negative for CD207/langerin. Fluorescence in situ hybridization using NCOA2 break‐apart probes confirmed a chromosomal break occurring on NCOA2 monoallele in the tumor cells. Furthermore, ETV3 exon 4‐NCOA2 exon 14 translocation was identified in formalin‐fixed paraffin‐embedded skin samples using reverse transcription polymerase chain reaction and subsequent direct DNA sequencing. He also presented with interspersed eczematous plaques on his trunk and reactive dermatopathic lymphoadenopathy without any infiltration of ICH. He was treated with topical corticosteroids and narrowband UVB phototherapy. Four months later, his ICH skin eruptions, eczematous plaques, and lymphoadenopathy gradually regressed. Our case supports the notion that the detection of ETV3‐NCOA2 translocation can be useful for diagnosis of ICH.

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CLEC4K

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