Transforming growth factor beta articles within Nature Communications

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  • Article
    | Open Access

    Age-related osteoporosis is known to be dependent on TGFβ1 signalling. Here the authors show that a subset of neutrophils (identified by TGFβ1+CCR5+) increase during aging in mouse bone marrow resulting in bone loss, while a CCR5 antagonist can reduce the neutrophil numbers and increase bone mass in aged mice.

    • Jinbo Li
    • , Zhenqiang Yao
    •  & Brendan F. Boyce

  • Article
    | Open Access

    TGF-β has been shown to regulate stem-like CD8 + T cell differentiation into tissue resident memory T cells in chronic infection. Here authors show that in tumour-bearing mice, a similar TGF-βdependent CD8 + T cell differentiation program is carried out in the draining lymph nodes, which impedes generation of anti-tumor migratory effector T cells upon future vaccination.

    • Guo Li
    • , Saranya Srinivasan
    •  & Nu Zhang

  • Article
    | Open Access

    Understanding the factors that hamper immune therapy in breast cancer may increase the range of patients who benefit. Here authors show that breast cancer cells produce and subsequently transfer active TGF-β type II receptors to CD8 + T cells to render them exhausted, thus paralyzing the anti-tumor immune response.

    • Feng Xie
    • , Xiaoxue Zhou
    •  & Fangfang Zhou

  • Article
    | Open Access

    CD4+ T helper cells producing IL-17A (TH17 cells) can take on pathogenic or anti-inflammatory functions in context-specific manners. Here the authors show that the anti-inflammatory fate of TH17 cells contributes, via TGF-β signaling and induction of IL-10, to host immune tolerance, but also simultaneously dampens protective immunity against S. aureus.

    • Hao Xu
    • , Theodora Agalioti
    •  & Nicola Gagliani

  • Article
    | Open Access

    The molecular basis of activin receptor-like kinase 1 (ALK1)-mediated endothelial bone morphogenetic protein (BMP) signalling is not fully understood. Here, the authors present crystal structures of the BMP10:ALK1 and prodomain-bound BMP9:ALK1 complexes, providing mechanistic insights into ALK1 signalling specificity.

    • Richard M. Salmon
    • , Jingxu Guo
    •  & Wei Li

  • Article
    | Open Access

    Aberrant tissue repair may result in heterotopic ossification (HO), but how this process is regulated by local inflammatory responses is still unclear. Here the authors show, using a mouse burn/trauma model, that TGFβ-producing monocytes/macrophages at the injury site contribute to HO induction, while CD47 activation helps antagonize this process.

    • Michael Sorkin
    • , Amanda K. Huber
    •  & Benjamin Levi

  • Article
    | Open Access

    TGF-β is thought to be important for group 2 innate lymphoid cell (ILC2) function. Here the authors show that TGF-β drives expression of ST2 specifically in ILC2 progenitors and thereby is also important for the development of ILC2s in the bone marrow.

    • Li Wang
    • , Jun Tang
    •  & WanJun Chen

  • Article
    | Open Access

    Idiopathic pulmonary fibrosis is associated with myofibroblast activation in the lungs and metabolic alterations. Here, the authors show that the antidiabetic drug metformin has antifibrotic effects in human-derived samples and mouse models, by modulating a number of metabolic pathways to induce lipogenic transdifferentiation of myofibroblasts.

    • Vahid Kheirollahi
    • , Roxana M. Wasnick
    •  & Elie El Agha

  • Article
    | Open Access

    The PI3K/Akt/mTOR pathway has been previously implicated in fibrosis and a pan-PI3K/mTOR inhibitor is currently under clinical evaluation for the treatment of IPF. Here the authors show that the mTORC1/4E-BP1 axis is critical for TGF-β1-induced fibrogenesis in in vitro and ex vivo models and that canonical PI3K/Akt signalling is dispensable.

    • Hannah V. Woodcock
    • , Jessica D. Eley
    •  & Rachel C. Chambers

  • Article
    | Open Access

    Studying the uterine lymphocyte pool is difficult due to its dynamic nature induced by various pregnancy-related factors. Here the authors provide, using transcriptome data from sorted mouse group 1 innate lymphoid cells (ILC), a molecular atlas of these cells, which implicates tissue-resident natural killer cells as a hub for uterine immune crosstalk.

    • Iva Filipovic
    • , Laura Chiossone
    •  & Francesco Colucci

  • Article
    | Open Access

    Hyperactivation of TGFβ signaling is a common feature of fibrotic diseases. Here the authors show that genetic or pharmacologic inactivation of the tyrosine phosphatase SHP2 prevents TGFβ-induced JAK2/STAT3 signaling, inhibits fibroblast activation and exerts potent anti-fibrotic effects.

    • Ariella Zehender
    • , Jingang Huang
    •  & Jörg H. W. Distler

  • Article
    | Open Access

    Feingold syndrome is a skeletal dysplasia caused by mutations in MYCN or MIR17HG, but it is not clear if these mutations lead to pathology via a common molecular mechanism. Here, the authors show that mutations in MIR17HG lead to upregulated TGF-β signaling in limb mesenchymal cells, while mutations in MYCN downregulate PI3K signaling.

    • Fatemeh Mirzamohammadi
    • , Anastasia Kozlova
    •  & Tatsuya Kobayashi

  • Article
    | Open Access

    Heterotopic ossification (HO) is a painful disease of unknown etiology characterized by extraskeletal bone formation after injury. Here the authors show that TGF-β is increased in HO lesions, where it promotes the early stages of HO pathology, and demonstrate that TGF-β inhibition ameliorates HO in mice.

    • Xiao Wang
    • , Fengfeng Li
    •  & Xu Cao

  • Article
    | Open Access

    Heligmosomoides polygyrus can activate mammalian TGF-β signalling pathways, but how it does so is not known. Here the authors identify and isolate a H. polygyrus TFG-β mimic that can bind both mammalian TGF-β receptor subunits, activate Smad signalling and generate inducible regulatory T cells.

    • Chris J. C. Johnston
    • , Danielle J. Smyth
    •  & Rick M. Maizels

  • Article
    | Open Access

    The mechanisms underlying tissue fibrosis are unclear. The authors show that mesenchymal cells expressing PDGFRβ mediate fibrosis in skeletal muscle and heart via a mechanism involving αv integrin, and that inhibitors of αv integrins attenuate fibrotic responses in mice.

    • I. R. Murray
    • , Z. N. Gonzalez
    •  & N. C. Henderson

  • Article
    | Open Access

    STAT3 is a transcription factor that is activated in fibrotic diseases such as systemic sclerosis. Here the authors show that STAT3 is the converging point for multiple pro-fibrotic signalling pathways, and that its genetic ablation or inhibition ameliorate skin fibrosis in mouse models.

    • Debomita Chakraborty
    • , Barbora Šumová
    •  & Jörg H. W. Distler

  • Article
    | Open Access

    Although protein tyrosine kinases are being explored as antifibrotic agents for the treatment of systemic sclerosis, little is known about the function of counteractive protein tyrosine phosphatases in this context. Here, the authors show that PTP4A1 is highly expressed by fibroblasts from patients with systemic sclerosis and promotes TGFβ activity via SRC–ERK–SMAD3 signaling.

    • Cristiano Sacchetti
    • , Yunpeng Bai
    •  & Nunzio Bottini

  • Article
    | Open Access

    Developmental cues for the different dendritic cell (DC) subsets in the intestine are yet to be defined. Here the authors show that TGFβR1 signalling is needed for development of CD103+CD11b+ intestinal DCs from CD103−CD11b+ cells and that they contribute to the generation of Th17 and regulatory T cells

    • C. C. Bain
    • , J. Montgomery
    •  & A. McI. Mowat

  • Article
    | Open Access

    Inhibition of GDF8 increases muscle mass in mice, but is less effective in monkeys and humans. Here the authors show that activin A also inhibits muscle hypertrophy and that concomitant inhibition of activin A and GDF8 synergistically increases muscle mass in mice and non-human primates.

    • Esther Latres
    • , Jason Mastaitis
    •  & Jesper Gromada

  • Article
    | Open Access

    Activins are members of the TGF-β family of growth factors that are processed from precursors into the mature proteins. Here, the authors use structural biology and biochemistry to examine the protein domain organisation and gain insights into the activation of pro-activin A.

    • Xuelu Wang
    • , Gerhard Fischer
    •  & Marko Hyvönen

  • Article |

    Colorectal cancer (CRC), like many solid tumours, progresses from adenomas to carcinomas in a sequence that leads to metastasis. Here the authors show that miR1269 plays a role in CRC relapse and metastasis by regulating TGF-β activity.

    • Pengcheng Bu
    • , Lihua Wang
    •  & Xiling Shen

  • Article
    | Open Access

    B cells reactive against self antigens can cause autoimmune disease, but are normally suppressed by regulatory T cells (Tregs). Here the authors show that a subset of Tregs can suppress lupus in a mouse model by making TGF-β3 cytokine and by engaging an inhibitory PD-1 receptor on B cells.

    • Tomohisa Okamura
    • , Shuji Sumitomo
    •  & Kazuhiko Yamamoto

  • Article |

    TGF-β signalling suppresses tumorigenesis in breast cancer cells but its effects on breast cancer initiating cells have not been reported. Using cells in culture, Brunaet al. show that TGF-β increases breast cancer initiating cell numbers in cells that have low levels of the tight junction protein claudin.

    • Alejandra Bruna
    • , Wendy Greenwood
    •  & Carlos Caldas

  • Article
    | Open Access

    Aberrant activation of the TGF-β pathway leads to fibrotic disease. Distler and colleagues show that TGF-β-mediated fibrosis requires the decrease of Dickkopf-1, an antagonist of canonical Wnt signalling, suggesting that the two pathways interact for the manifestation of this disease.

    • Alfiya Akhmetshina
    • , Katrin Palumbo
    •  & Jörg H.W. Distler

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