The role of TGF-β in growth, differentiation, and maturation of B lymphocytes

Lebman, Deborah A.; Edmiston, Jeffery

doi:10.1016/s1286-4579(99)00254-3

Cited by 139 publications

(93 citation statements)

References 61 publications

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“…TGFb is produced by FDCs, which are intimately associated with FL cells. 8,12,48,49 We observed that FDC-like cells, BMSCs and H2 cells released TGFb in the culture medium. In addition, TNFa, which is present in the FL microenvironment enhanced TGFb release by H2 cells.…”

Section: Tgfb-mediatedmentioning

confidence: 80%

“…[7][8][9][10] Through Smad1 and other Smad proteins, TGFb family members affects proliferation, survival and differentiation of normal and malignant cells, including lymphocytes. [11][12][13] This superfamily includes TGFb isoforms, activins (Acts) and bone morphogenetic proteins (BMPs). [14][15][16] The antiproliferative activity of TGFb, Acts and BMPs in lymphocytes is well established.…”

Section: Introductionmentioning

confidence: 99%

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TGFβ-mediated activation of Smad1 in B-cell non-Hodgkin's lymphoma and effect on cell proliferation

et al. 2004

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We have previously reported an overexpression of Smad1 in follicular lymphoma (FL) cells, which are characterized by the t(14;18) bcl2/IgH translocation. Smad1 is commonly involved in bone morphogenetic protein but not in tumor-transforming growth factor beta (TGFb) signaling pathways. This study focuses on Smad1 signaling pathway in non-Hodgkin lymphoma cells including follicular or large-cell lymphoma cells. Our results support the notion that phosphorylation of Smad1 is mediated by TGFb present in the microenvironment and occurs in FL in vivo. Using an in vitro coculture system mimicking interactions between stroma cells and FL cells, we found that both the cell partners release TGFb at a sufficient concentration to activate Smad pathways in the malignant cells. This Smad1 activation involves TGFbRII but not ALK-1 receptors, and does not compete with the Smad2 pathway. Moreover, proliferation assays performed on lymphoma cells expressing wild-type or mutated Smad1, or in which endogenous Smad1 level was decreased by gene silencing, strongly supported that overexpression and activation of Smad1 modifies the biological response of lymphoma B cells to TGFb family members. This work opens new insights into aberrant Smad pathways and their pathophysiological role in FL and in other non-Hodgkin lymphomas.

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Section: Tgfb-mediatedmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

TGFβ-mediated activation of Smad1 in B-cell non-Hodgkin's lymphoma and effect on cell proliferation

et al. 2004

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“…Tgfb1 encodes transforming growth factor b1 (TGF-b1), which acts in cell growth, differentiation, and apoptosis and plays an important role in controlling the immune system by regulating the expression of antibodies and MHC class II on B cells. (41) Few investigations have referred to the role of TGF-b1 in kidney stone formation. Tsujihata and colleagues (42) reported the inhibitory effect of atrovastatin on kidney stone formation and considered that the suppression of TGF-b1-induced tubular damage and interstitial fibrosis could be caused by the inhibition of renal tubular cell injury and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Renal macrophage migration and crystal phagocytosis via inflammatory-related gene expression during kidney stone formation and elimination in mice: Detection by association analysis of stone-related gene expression and microstructural observation

Okada

Yasui

Fujii

et al. 2010

Journal of Bone and Mineral Research

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Mice have a strong ability to eliminate renal calcium oxalate crystals, and our previous examination indicated a susceptibility in which monocyte-macrophage interaction could participate in the phenomenon. To clarify the macrophage-related factors playing roles in the prevention of crystal formation in mouse kidneys, morphologic and expression studies based on microarray pathway analysis were performed. Eight-week-old male C57BL/6N mice were administered 80 mg/kg of glyoxylate by daily intraabdominal injection for 15 days, and the kidneys were extracted every 3 days for DNA microarray analysis. Based on the raw data of microarray analysis, pathway analyses of inflammatory response demonstrated macrophage activation through the increased expression of chemokine (C-X-C) ligand 1, fibronectin 1, and major histocompatability (MHC) class II. Association analysis of related gene expression values by quantitative reverse transcription polymerase chain reaction (RT-PCR) indicated the high association of chemokine (C-C) ligand 2, CD44, colony-stimulating factor 1, fibronectin 1, matrix gla protein, secreted phosphoprotein 1, and transforming growth factor b1 (TGF-b1) with the amount of both renal crystals and F4/80, a macrophage marker. Immunohistochemically, interstitial macrophages increased during the experimental course, and CD44 and MHC class II were upregulated around crystal-formation sites. Ultrastructural observation of renal macrophages by transmission electron microscopy indicated interstitial macrophage migration with the phagocytosis of crystals. In conclusion, increased expression of inflammation-related genes of renal tubular cells induced by crystal formation and deposition could induce monocyte-macrophage migration and phagocytosis via the interaction of CD44 with osteopontin and fibronectin. Such crystalremoving ability of macrophages through phagocytosis and digestion might become a new target for the prevention of stone formation. ß

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“…In mammalian milk, TGF-b is present at high concentrations and may be a key immunoregulatory factor for promoting intestinal maturation (Rautava et al 2012), IgA production, and tolerance induction (Letterio et al 1994;Hawkes et al 1999;Kalliomaki et al 1999;Lebman and Edmiston 1999;Donnet-…”

Section: Development Of the Gut Barriermentioning

confidence: 99%

Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection

Sanjabi

2017

Cold Spring Harb Perspect Biol

452

306

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Transforming growth factor b (TGF-b) is a pleiotropic cytokine involved in both suppressive and inflammatory immune responses. After 30 years of intense study, we have only begun to elucidate how TGF-b alters immunity under various conditions. Under steady-state conditions, TGF-b regulates thymic T-cell selection and maintains homeostasis of the naïve T-cell pool. TGF-b inhibits cytotoxic T lymphocyte (CTL), Th1-, and Th2-cell differentiation while promoting peripheral ( p)Treg-, Th17-, Th9-, and Tfh-cell generation, and T-cell tissue residence in response to immune challenges. Similarly, TGF-b controls the proliferation, survival, activation, and differentiation of B cells, as well as the development and functions of innate cells, including natural killer (NK) cells, macrophages, dendritic cells, and granulocytes. Collectively, TGF-b plays a pivotal role in maintaining peripheral tolerance against self-and innocuous antigens, such as food, commensal bacteria, and fetal alloantigens, and in controlling immune responses to pathogens.

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The role of TGF-β in growth, differentiation, and maturation of B lymphocytes

Cited by 139 publications

References 61 publications

TGFβ-mediated activation of Smad1 in B-cell non-Hodgkin's lymphoma and effect on cell proliferation

TGFβ-mediated activation of Smad1 in B-cell non-Hodgkin's lymphoma and effect on cell proliferation

Renal macrophage migration and crystal phagocytosis via inflammatory-related gene expression during kidney stone formation and elimination in mice: Detection by association analysis of stone-related gene expression and microstructural observation

Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection

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