Adipocytes as immune cells: differential expression of TWEAK, BAFF, and APRIL and their receptors (Fn14, BAFF-R, TACI, and BCMA) at different stages of normal and pathological adipose tissue development.
Adipose tissue represents a rich source of multipotent stem cells. Mesenchymal cells, isolated from this source, can differentiate to other cell types in vitro and therefore can be used for a number of regenerative therapies. Our view of adipose tissue has recently changed, establishing adipocytes as new members of the immune system, as they produce a number of proinflammatory cytokines (such as IL-6 and TNFalpha and chemokines, in addition to adipokines (leptin, adiponectin, resistin) and molecules associated with the innate immune system. In this paper, we report the differential expression of TNF-superfamily members B cell activating factor of the TNF Family (BAFF), a proliferation inducing ligand (APRIL), and TNF-like weak inducer of apoptosis (TWEAK) in immature-appearing and mature adipocytes and in benign and malignant adipose tissue-derived tumors. These ligands act through their cognitive receptors, BAFF receptor, transmembrane activator and calcium signal-modulating cyclophilic ligand (TACI), B cell maturation Ag (BCMA), and fibroblast growth factor-inducible 14 (Fn14), which are also expressed in these cells. We further report the existence of functional BCMA, TACI, and Fn14 receptors and their ligands BAFF, APRIL, and TWEAK on adipose tissue-derived mesenchymal cells, their interaction modifying the rate of adipogenesis. Our data integrate BAFF, APRIL, and TWEAK and their receptors BCMA, TACI, and Fn14 as novel potential mediators of adipogenesis, in addition to their specific role in immunity, and define immature and mature adipocytes as source of immune mediators.
Alexaki
Vassilia-Ismini
VI
Department of Experimental Endocrinology, University of Crete, School of Medicine, Heraklion, Greece.
Notas
George
G
Pelekanou
Vassiliki
V
Kampa
Marilena
M
Valkanou
Maria
M
Theodoropoulos
Panayiotis
P
Stathopoulos
Efstathios N
EN
Tsapis
Andreas
A
Castanas
Elias
E
D017667:Adipocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D000273:Adipose Tissue / Q000166:cytology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D053264:B-Cell Activating Factor / Q000096:biosynthesis*; D053265:B-Cell Activation Factor Receptor / Q000096:biosynthesis*; D053301:B-Cell Maturation Antigen / Q000096:biosynthesis*; D002454:Cell Differentiation / Q000276:immunology; D002478:Cells, Cultured; D000074049:Cytokine TWEAK; D006801:Humans; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis*; D000074050:TWEAK Receptor; D053303:Transmembrane Activator and CAML Interactor Protein / Q000096:biosynthesis*; D014407:Tumor Cells, Cultured; D053300:Tumor Necrosis Factor Ligand Superfamily Member 13 / Q000096:biosynthesis*; D048069:Tumor Necrosis Factors / Q000096:biosynthesis*
D053264:B-Cell Activating Factor; D053265:B-Cell Activation Factor Receptor; D053301:B-Cell Maturation Antigen; D000074049:Cytokine TWEAK; D018124:Receptors, Tumor Necrosis Factor; C000613297:TNFRSF12A protein, human; C108467:TNFRSF13B protein, human; C435926:TNFRSF13C protein, human; C086966:TNFRSF17 protein, human; C109743:TNFSF12 protein, human; C505719:TNFSF13B protein, human; D000074050:TWEAK Receptor; D053303:Transmembrane Activator and CAML Interactor Protein; D053300:Tumor Necrosis Factor Ligand Superfamily Member 13; D048069:Tumor Necrosis Factors