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Last update 08 May 2025

XCL1

Last update 08 May 2025

Basic Info

Synonyms

ATAC, C motif chemokine 1, Cytokine SCM-1

+ [12]

Introduction

Chemotactic activity for lymphocytes but not for monocytes or neutrophils. In thymus, mediates medullary accumulation of thymic dendritic cells and contributes to regulatoy T cell development, playing a role in self-tolerance establishment.

Drugs associated with XCL1

CN118178615

Patent Mining

Target

XCL1

Mechanism-

Active Org.

Southern Medical University

Originator Org.

Southern Medical University

Active Indication

pregnancy late [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with XCL1

100 Translational Medicine associated with XCL1

0 Patents (Medical) associated with XCL1

565

Literatures (Medical) associated with XCL1

08 Apr 2025·JCI Insight

The XCL1/XCR1 axis is upregulated in type 1 diabetes and aggravates its pathogenesis

Article

Author: Hintermann, Edith ; Bachmann, Malte ; Brandes, Ralf P ; Puppe, Deborah ; Kroczek, Richard A ; Pfeilschifter, Josef ; Bender, Christine ; Christen, Urs ; Betts, Michael R ; Tondello, Camilla ; Bayer, Monika ; Blickberndt, Elisa ; Golden, Gregory J ; Buchmann, Giulia K

Type 1 diabetes (T1D) is precipitated by the autoimmune destruction of the insulin-producing β cells in the pancreatic islets of Langerhans. Chemokines have been identified as major conductors of islet infiltration by autoaggressive leukocytes, including antigen-presenting cells and islet autoantigen-specific T cells. We have previously generated a road map of gene expression in the islet microenvironment during T1D in a mouse model and found that most of the chemokine axes are chronically upregulated during T1D. The XCL1/XCR1 chemokine axis is of particular interest, since XCR1 is exclusively expressed on conventional DCs type 1 (cDC1) that excel by their high capacity for T cell activation. Here, we demonstrate that cDC1-expressing XCR1 are present in and around the islets of patients with T1D and of individuals with islet autoantibody positivity. Furthermore, we show that XCL1 plays an important role in the attraction of highly potent DCs expressing XCR1 to the islets in an inducible mouse model for T1D. XCL1-deficient mice display a diminished infiltration of XCR1+ cDC1 and, subsequently, a reduced magnitude and activity of islet autoantigen-specific T cells, resulting in a profound decrease in T1D incidence. Interference with the XCL1/XCR1 chemokine axis might constitute a novel therapy for T1D.

01 Apr 2025·SLAS Technology

Systemic trafficking of macrophages in implant wear debris-induced periprosthetic osteolysis

Review

Author: Lou, Mengyun

Periprosthetic osteolysis (PPOL) is a significant complication post-joint replacement, often instigated by implant wear debris, leading to chronic inflammation and bone resorption. Herein, this review summarizes the immune mechanisms of PPOL, specifically, the processes where macrophages are recruited by implant wear debris, the mechanisms by which macrophages trigger inflammatory cascades, and the role of chemokines that facilitate macrophage migration, including CCL2, CCL3, CCL4, CCL5, CXCL8, CX3CL1, and XCL1. This review highlights novel findings on these processes and suggests that illustrating these mechanisms offers promising avenues for future therapeutic strategies to prevent and treat PPOL, such as the potential use of anti-inflammatory drugs.

03 Mar 2025·Journal of Experimental Medicine

The XCL1–XCR1 axis supports intestinal tissue residency and antitumor immunity

Article

Author: Goldrath, Ananda W. ; Reina-Campos, Miguel ; Schokrpur, Shiruyeh ; Scharping, Nicole E. ; Kuo, Ning ; Mempel, Kianoosh M. ; Ferry, Amir ; Monell, Alexander ; Saddawi-Konefka, Robert ; Gutkind, J. Silvio ; Takehara, Kennidy K. ; Heeg, Maximilian

Tissue-resident memory T cells (TRM) provide frontline protection against pathogens and emerging malignancies. Tumor-infiltrating lymphocytes (TIL) with TRM features are associated with improved clinical outcomes. However, the cellular interactions that program TRM differentiation and function are not well understood. Using murine genetic models and targeted spatial transcriptomics, we found that the CD8+ T cell–derived chemokine XCL1 is critical for TRM formation and conventional DC1 (cDC1) supported the positioning of intestinal CD8+ T cells during acute viral infection. In tumors, enforced Xcl1 expression by antigen-specific CD8+ T cells promoted intratumoral cDC1 accumulation and T cell persistence, leading to improved overall survival. Notably, analysis of human TIL and TRM revealed conserved expression of XCL1 and XCL2. Thus, we have shown that the XCL1–XCR1 axis plays a non-cell autonomous role in guiding intestinal CD8+ TRM spatial differentiation and tumor control.

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