HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4

By M. Schiraldi, A. Raucci, L. Muñoz, Elsa Livoti, Barbara Celona, E. Vénéreau, Tiziana Apuzzo, F. De Marchis, M. Pedotti, A. Bachi and 6 more. Journal of Experimental Medicine, 2012

644 citations recorded by the source corpus.

CXCL12 forms a complex with HMGB1 that binds to the chemokine receptor CXCR4 and increases inflammatory cell migration.

Subfields: Clinical Biochemistry, Immunology

View Paper: https://www.semanticscholar.org/paper/50f489a65986ac44f5167bafacdf531298af2bea

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. A. Rubartelli
2. A. Manfredi
3. Peter Vandenabeele
4. Nikolaos G. Frangogiannis

In Immunology

1. Guido Kroemer
2. L. Zitvogel
3. L. Galluzzi
4. M. Smyth
5. Oliver Kepp
6. S. Formenti
7. S. Demaria
8. A. Buqué

Citations in the corpus

• International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the Extended Family of Chemokine Receptors and Introducing a New Nomenclature for Atypical Chemokine Receptors (2014, neutral): “It binds CXCL12 and shifts the efficiency of CXCR4 activation to lower concentrations of CXCL12 (Schiraldi et al., 2012).”
• Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti–PD-L1 immunotherapy in pancreatic cancer (2013, background): “We hypothesize that high mobility group box 1 (HMGB1), which is overexpressed and secreted by metabolically stressed cancer cells (17), captures CXCL12 by forming a high-affinity heterocomplex (18), thus explaining the paradoxical localization of CXCL12 on cancer cells despite their not producing CX”
• The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “the formation of HMGB1-CXCL12 heterocomplexes that synergistically enhance CXCR4 signaling in inflammatory cells.(30)”
• Oxidant Mechanisms in Renal Injury and Disease (2016, positive): “If these cysteine residues are reduced thiols, then circulating HMGB1 induces repair of the injured tissues (272,310).”
• Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “The concept of CXCR4-dependent release of neutrophils from the bone marrow has recently been challenged by an intravital microscopy study showing that CXCR4 inhibition using plerixafor in mice triggers mobilization of neutrophils from the marginated pool of the lung and simultaneously prevents neutr”
• The Chemokine Superfamily Revisited (2012, positive): “Finally, the nuclear protein HMGB1 can also interact with CXCL12 and mediates mononuclear cell recruitment in vivo via CXCR4 (Schiraldi et al., 2012).”
• Consensus guidelines for the detection of immunogenic cell death (2014, background): “Moreover, extracellular HMGB1 reportedly exerts a chemotactic activity by forming a complex with chemokine (C-X-C motif) ligand 12 (CXCL12) that signals via chemokine (C-X-C motif) receptor 4 (CXCR4).(211) Finally, at least under some circumstances, endogenous HMGB1 appears to promote autophagy by i”