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Dysregulation of DPP4-CXCL12 Balance by TGF-β1/SMAD Pathway Promotes CXCR4+ Inflammatory Cell Infiltration in Keloid Scars

https://doi.org/10.2147/jir.s326385
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25/25 checkable references clean · checked 2026-07-23

Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.

The 25 checked references that resolve
resolves10.3390/ijms18030606
Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis
resolves10.1111/j.1365-2133.2012.11190.x
Site-specific immunophenotyping of keloid disease demonstrates immune upregulation and the presence of lymphoid aggregates
resolves10.1097/PRS.0000000000005717
The Interplay of Mechanical Stress, Strain, and Stiffness at the Keloid Periphery Correlates with Increased Caveolin-1/ROCK Signaling and Scar Progression
resolves10.1159/000491924
Spontaneous Keloids: A Literature Review
resolves10.1016/j.jid.2018.07.044
NEDD4 Is Involved in Inflammation Development during Keloid Formation
resolves10.1189/jlb.3MR0915-401R
CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology
resolves10.1038/ni.3201
Dipeptidylpeptidase 4 inhibition enhances lymphocyte trafficking, improving both naturally occurring tumor immunity and immunotherapy
resolves10.1007/s10753-019-01148-1
IL-17 Induced Stromal Cell–Derived Factor-1 and Profibrotic Factor in Keloid-Derived Skin Fibroblasts via the STAT3 Pathway
resolves10.1016/j.jid.2015.11.008
TSLP Is a Potential Initiator of Collagen Synthesis and an Activator of CXCR4/SDF-1 Axis in Keloid Pathogenesis
resolves10.1038/sj.jid.5700069
Involvement of the CXCL12/CXCR4 Pathway in the Recovery of Skin Following Burns
resolves10.1016/j.jid.2016.12.028
Misbalanced CXCL12 and CCL5 Chemotactic Signals in Vitiligo Onset and Progression
resolves10.1073/pnas.1612900114
PLCε1 regulates SDF-1α–induced lymphocyte adhesion and migration to sites of inflammation
resolves10.1089/scd.2016.0026
Modulation of Hematopoietic Chemokine Effects In Vitro and In Vivo by DPP-4/CD26
resolves10.1007/s13361-013-0822-7
Quantification of Intact and Truncated Stromal Cell-Derived Factor-1α in Circulation by Immunoaffinity Enrichment and Tandem Mass Spectrometry
resolves10.1111/j.1365-2222.2011.03778.x
Dipeptidyl peptidase IV (DPP4) deficiency increases Th1-driven allergic contact dermatitis
resolves10.1093/ejcts/ezr180
CD26/DPP-4 inhibition recruits regenerative stem cells via stromal cell-derived factor-1 and beneficially influences ischaemia-reperfusion injury in mouse lung transplantation
resolves10.1182/blood-2005-04-1492
Skin homing of Sézary cells involves SDF-1-CXCR4 signaling and down-regulation of CD26/dipeptidylpeptidase IV
resolves10.1111/bjd.16173
Characterization of CD45RO+ memory T lymphocytes in keloid disease
resolves10.1073/pnas.1013805107
Autocrine TGF-β and stromal cell-derived factor-1 (SDF-1) signaling drives the evolution of tumor-promoting mammary stromal myofibroblasts
resolves10.1002/cam4.2249
CD26 expression is attenuated by TGF‐β and SDF‐1 autocrine signaling on stromal myofibroblasts in human breast cancers
resolves10.1111/bjd.14720
The prognostic significance and impact of the CXCR4-CXCR7-CXCL12 axis in primary cutaneous melanoma
resolves10.1016/j.jid.2017.02.012
Alterations of CXCL12 in Serum of Patients with Vitiligo
resolves10.1016/j.jaci.2015.07.037
Number, activation, and differentiation of circulating fibrocytes correlate with asthma severity
resolves10.1016/j.jid.2020.04.010
CD26 Identifies a Subpopulation of Fibroblasts that Produce the Majority of Collagen during Wound Healing in Human Skin
resolves10.1126/science.aaa2151
Identification and isolation of a dermal lineage with intrinsic fibrogenic potential
What this badge says. CiteStamped means the CHECKABLE references of this work were clean at the dated check: each resolved to a known work in a public registry, and none carried a retraction notice at that time. It says nothing about the quality, findings, or importance of the work itself, and nothing about references deposited without a DOI.

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