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C1q and HMGB1 reciprocally regulate human macrophage polarization

Son, Myoungsun ; Porat, Amit ; He, Mingzhu ; Suurmond, Jolien ; Santiago-Schwarz, Frances ; Andersson, Ulf ; Coleman, Thomas R. ; Volpe, Bruce T. ; Tracey, Kevin J. ; Al-Abed, Yousef ; Diamond, Betty

Blood, 2016-11, Vol.128 (18), p.2218-2228 [Revista revisada por pares]

United States: Elsevier Inc

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Título:
C1q and HMGB1 reciprocally regulate human macrophage polarization
Autor: Son, Myoungsun ; Porat, Amit ; He, Mingzhu ; Suurmond, Jolien ; Santiago-Schwarz, Frances ; Andersson, Ulf ; Coleman, Thomas R. ; Volpe, Bruce T. ; Tracey, Kevin J. ; Al-Abed, Yousef ; Diamond, Betty
Materias: Cell Differentiation - immunology ; Cell Polarity ; Complement C1q - immunology ; Complement C1q - metabolism ; HMGB1 Protein - immunology ; HMGB1 Protein - metabolism ; Humans ; Immunobiology ; Macrophages - cytology ; Macrophages - immunology ; Macrophages - metabolism ; Medicin och hälsovetenskap ; Signal Transduction - immunology
Es parte de: Blood, 2016-11, Vol.128 (18), p.2218-2228
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
M.S. and A.P. contributed equally to this study.
Descripción: A healthy immune system results from a balance of stimulatory and inhibitory pathways that allow effective responses to acute insults, without descending into chronic inflammation. Failed homeostasis is characteristic of autoimmune diseases such as systemic lupus erythematosus. Although HMGB1 induces proinflammatory M1-like macrophage differentiation, we describe a mechanism by which C1q modulates this activity and collaborates with HMGB1 to induce the differentiation of monocytes to anti-inflammatory M2-like macrophages. These anti-inflammatory macrophages are unresponsive to dendritic cell induction factors, effectively removing them from participation in an adaptive immune response. This pathway is mediated through a complex with RAGE and LAIR-1 and depends on relative levels of C1q and HMGB1. Importantly, these data provide insight into a homeostatic mechanism in which C1q and HMGB1 can cooperate to terminate inflammation, and which may be impaired in C1q-deficient patients with autoimmune disease. •C1q can form a multimolecular signaling complex with HMGB1, RAGE, and LAIR-1 in lipid rafts.•C1q and HMGB1 together promote monocytes to differentiate to an anti-inflammatory phenotype.
Editor: United States: Elsevier Inc
Idioma: Inglés

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C1q and HMGB1 reciprocally regulate human macrophage polarization

Son, Myoungsun ; Porat, Amit ; He, Mingzhu ; Suurmond, Jolien ; Santiago-Schwarz, Frances ; Andersson, Ulf ; Coleman, Thomas R. ; Volpe, Bruce T. ; Tracey, Kevin J. ; Al-Abed, Yousef ; Diamond, Betty

United States: Elsevier Inc

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