About this Research Topic
Although gC1qR was first identified as a receptor for C1q in 1992, a large body of structural and functional information accumulated to date has shown that it is a multifunctional receptor that can activate or inhibit several signaling pathways. It has a ubiquitous cellular distribution with mitochondrial, cytoplasmic and cell surface localization, as well as secreted forms. It binds to several proteins present in plasma, on the cell surface, intracellular or proteins encoded by pathogens. Thus, gC1qR plays a critical role in immunity against microbes such as HIV, HCV, Staphylococcus aureus, Porphyromonas gingivalis and also tumors. For example, the 3S motif of HIV gp41 protein, binds to gC1qR to increase PLA2G1B-driven inhibition of CD4 T-cell function in HIV-infected patients. This 3S motif is highly conserved across species and is shared by several pathogenic microorganisms, including those that are known to be associated with the development of cancer, along with various other types of disease.
gC1qR, also known as: p33, p32, and hyaluronic acid binding protein (HABP1), is encoded by the C1QBP gene, and modulates a plethora of immunological processes including those involved in infection, inflammation, autoimmunity and cancer. Due to its critical role in these diseases, gC1qR has become a suitable candidate for the development of therapeutic modalities against infection and cancer. The multifunctional role of gC1qR in the regulation of immune responses in turn, is due to its ability to bind to multiple endogenous or exogenous components. Amongst the endogenous components that bind gC1qR and regulate immune responses are C1q, the surface co-receptor DC-SIGN (CD209), and the mitochondrial antiviral signaling (MAVS) protein. In addition, gC1qR serves as a pathogen recognition receptor by virtue of its ability to bind to numerous pathogen-associated molecules, including bacterial, parasitic and viral ligands. These ligands have been shown to be involved in various infections, as well as oncogenesis. The aim of this Research Topic is therefore to reveal the advances that have been made in our efforts to understand the role of gC1qR in these diseases and provide a rationale as to why gC1qR is a suitable target for the development of therapeutic options against infection and cancer.
This Research Topic aims to provide current information to immunologists, microbiologists, oncologists and clinicians, about the role of gC1qR in immunity against pathogens and tumors.
We welcome Mini Review, Perspectives, Systematic Review (including meta-analyses) and Original Research (basic research, pre-clinical, translational, and clinical research) articles related to, but not limited to, the following topics:
- Characterization of the mode of action of gC1qR in the regulation of immune responses against pathogens or tumors
- Identification of the binding motif of endogenous or exogenous components to gC1qR involved in the regulation of immune responses
- The effect of ligand binding to gC1qR on downstream signaling (gene expression, protein expression or metabolism) in immune cells
- Omics studies that focus on the role of gC1qR in immunity against pathogens or tumors at transcriptomic, proteomic or metabolomic levels in immune cells
- Investigation of the potential of therapeutic candidates targeting gC1qR to treat infections or tumors
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
gC1qR, also known as: p33, p32, and hyaluronic acid binding protein (HABP1), is encoded by the C1QBP gene, and modulates a plethora of immunological processes including those involved in infection, inflammation, autoimmunity and cancer. Due to its critical role in these diseases, gC1qR has become a suitable candidate for the development of therapeutic modalities against infection and cancer. The multifunctional role of gC1qR in the regulation of immune responses in turn, is due to its ability to bind to multiple endogenous or exogenous components. Amongst the endogenous components that bind gC1qR and regulate immune responses are C1q, the surface co-receptor DC-SIGN (CD209), and the mitochondrial antiviral signaling (MAVS) protein. In addition, gC1qR serves as a pathogen recognition receptor by virtue of its ability to bind to numerous pathogen-associated molecules, including bacterial, parasitic and viral ligands. These ligands have been shown to be involved in various infections, as well as oncogenesis. The aim of this Research Topic is therefore to reveal the advances that have been made in our efforts to understand the role of gC1qR in these diseases and provide a rationale as to why gC1qR is a suitable target for the development of therapeutic options against infection and cancer.
This Research Topic aims to provide current information to immunologists, microbiologists, oncologists and clinicians, about the role of gC1qR in immunity against pathogens and tumors.
We welcome Mini Review, Perspectives, Systematic Review (including meta-analyses) and Original Research (basic research, pre-clinical, translational, and clinical research) articles related to, but not limited to, the following topics:
- Characterization of the mode of action of gC1qR in the regulation of immune responses against pathogens or tumors
- Identification of the binding motif of endogenous or exogenous components to gC1qR involved in the regulation of immune responses
- The effect of ligand binding to gC1qR on downstream signaling (gene expression, protein expression or metabolism) in immune cells
- Omics studies that focus on the role of gC1qR in immunity against pathogens or tumors at transcriptomic, proteomic or metabolomic levels in immune cells
- Investigation of the potential of therapeutic candidates targeting gC1qR to treat infections or tumors
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Keywords: gC1qR, Tumour, Anti-Tumour, Immune Response
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.
