Requirement of HMGB1 for stromal cell-derived factor-1/CXCL12-dependent migration of macrophages and dendritic cells
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Requirement of HMGB1 for stromal cell-derived factor-1/CXCL12-dependent migration of macrophages and dendritic cells. / Campana, L.; Bosurgi, L.; Bianchi, M.E.; Manfredi, A.A.; Rovere-Querini, P.
in: J LEUKOCYTE BIOL, Jahrgang 86, Nr. 3, 2009, S. 609-15.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Requirement of HMGB1 for stromal cell-derived factor-1/CXCL12-dependent migration of macrophages and dendritic cells
AU - Campana, L.
AU - Bosurgi, L.
AU - Bianchi, M.E.
AU - Manfredi, A.A.
AU - Rovere-Querini, P.
PY - 2009
Y1 - 2009
N2 - HMGB1 finely tunes the function of DCs, thus influencing their maturation program and eventually the establishment of adaptive, T cell-dependent immune responses. Moreover, it promotes the up-regulation of receptors for lymph node chemokines, regulates the remodeling of the cytoskeleton of migrating cells, and sustains their journey to secondary lymphoid organs via a RAGE-dependent pathway. The inflammatory properties of HMGB1 depend at least partially on the ability to complex with soluble moieties, including nucleic acids, microbial products, and cytokines. Here, we show that bone marrow-derived mouse DCs release HMGB1 during CXCL12-dependent migration in vitro. Macrophages share this property, suggesting that it may be a general feature of CXCL12-responsive leukocytes. The chemotactic response to rCXCL12 of DCs and macrophages abates in the presence of the HMGB1 antagonist BoxA. HMGB1 secreted from DCs and macrophages binds to CXCL12 in the fluid phase and protects the chemokine conformation and function in a reducing environment. Altogether, our data indicate that HMGB1 release is required for CXCL12 ability to attract myeloid-derived cells and reveal a functional interaction between the two molecules that possibly contributes to the regulation of leukocyte recruitment and motility.
AB - HMGB1 finely tunes the function of DCs, thus influencing their maturation program and eventually the establishment of adaptive, T cell-dependent immune responses. Moreover, it promotes the up-regulation of receptors for lymph node chemokines, regulates the remodeling of the cytoskeleton of migrating cells, and sustains their journey to secondary lymphoid organs via a RAGE-dependent pathway. The inflammatory properties of HMGB1 depend at least partially on the ability to complex with soluble moieties, including nucleic acids, microbial products, and cytokines. Here, we show that bone marrow-derived mouse DCs release HMGB1 during CXCL12-dependent migration in vitro. Macrophages share this property, suggesting that it may be a general feature of CXCL12-responsive leukocytes. The chemotactic response to rCXCL12 of DCs and macrophages abates in the presence of the HMGB1 antagonist BoxA. HMGB1 secreted from DCs and macrophages binds to CXCL12 in the fluid phase and protects the chemokine conformation and function in a reducing environment. Altogether, our data indicate that HMGB1 release is required for CXCL12 ability to attract myeloid-derived cells and reveal a functional interaction between the two molecules that possibly contributes to the regulation of leukocyte recruitment and motility.
UR - http://www.scopus.com/inward/record.url?eid=2-s2.0-70149092553&partnerID=MN8TOARS
U2 - 10.1189/jlb.0908576
DO - 10.1189/jlb.0908576
M3 - SCORING: Journal article
C2 - 19414537
VL - 86
SP - 609
EP - 615
JO - J LEUKOCYTE BIOL
JF - J LEUKOCYTE BIOL
SN - 0741-5400
IS - 3
ER -
