About this Research Topic
The TGF-beta superfamily molecules, including TGFs, activins, BMPs, GDFs and Nodals, form the largest family of growth and differentiation factors, and are highly conserved among animals. They regulate diverse developmental and physiological processes, including tissue homeostasis and cell fate. The cytokine TGF-beta is well-known for its role in regulation of immune responses and tissue fibrosis, but recently important immune functions have been identified for other TGF-beta superfamily members, such as activin A and the BMPs. Signalling is via interaction with receptor complexes formed of transmembrane type I receptors and type II serine/threonine kinase receptors, leading to phosphorylation of Smads and subsequent initiation of transcription. Differences in the functions of TGF-beta superfamily ligands are achieved by the combinatorial diversity of type I and II receptors in the receptor complexes, and the interaction of Smads with multiple transcription factors, co-activators and co-repressors, as well as signaling through non-canonical pathways.
While mounting evidence suggests important roles for TGF-beta superfamily cytokines such as activin A and BMPs in immune responses, there have been limited studies on the role of these cytokines in disease, particularly in infectious disease. This is partially because deletion is typically embryonically lethal. In addition, these proteins are synthesized as precursors that require cleavage, and their role in diseases may be overlooked in transcriptomic approaches. However, advances in genetic technology that allow the use of conditional, overexpressing or cell-specific mutants, silencing RNA and CRISPR/Cas9 and the use of specific inhibitors have potential to reveal previously unknown roles for these molecules.
In this Research topic, we welcome original research articles, review articles, meta-analyses, and clinical trials focusing on the role of TGF-beta superfamily members in immunity and disease, including but not limited to:
• Signaling pathways of TGF-beta superfamily members
• Modulation of immune responses by TGF-beta superfamily members
• Roles of TGF-beta superfamily members in infectious disease, autoimmunity, allergy, inflammation and cancer
• Tools and models for investigating functions of TGF-beta superfamily members
• Profiles of TGF-beta superfamily expression in different diseases
• Targeting of TGF-beta superfamily molecules for host-directed therapy, e.g. cancer immunotherapy
While mounting evidence suggests important roles for TGF-beta superfamily cytokines such as activin A and BMPs in immune responses, there have been limited studies on the role of these cytokines in disease, particularly in infectious disease. This is partially because deletion is typically embryonically lethal. In addition, these proteins are synthesized as precursors that require cleavage, and their role in diseases may be overlooked in transcriptomic approaches. However, advances in genetic technology that allow the use of conditional, overexpressing or cell-specific mutants, silencing RNA and CRISPR/Cas9 and the use of specific inhibitors have potential to reveal previously unknown roles for these molecules.
In this Research topic, we welcome original research articles, review articles, meta-analyses, and clinical trials focusing on the role of TGF-beta superfamily members in immunity and disease, including but not limited to:
• Signaling pathways of TGF-beta superfamily members
• Modulation of immune responses by TGF-beta superfamily members
• Roles of TGF-beta superfamily members in infectious disease, autoimmunity, allergy, inflammation and cancer
• Tools and models for investigating functions of TGF-beta superfamily members
• Profiles of TGF-beta superfamily expression in different diseases
• Targeting of TGF-beta superfamily molecules for host-directed therapy, e.g. cancer immunotherapy
Keywords: TGF-beta superfamily, activin A, bone morphogenetic proteins (BMPs), growth/differentiation factors (GDFs), Nodals, Anti-müllerian hormone (AMH), Smad, cytokines, infection, immunity, cancer, allergy, inflammation, T cell, Treg, TGF-beta
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
