About this Research Topic
The innate immune system comprises of a group of cellular receptors termed as Pathogen recognition receptors (PRRs) which recognize common microbial patterns and danger signals and activate signaling cascades that result in a cytokine response against the invading pathogens. The nucleotide binding and oligomerization domain (NOD)-like receptors (NLRs) comprises a group of evolutionarily conserved intracellular PRRs. The NLR family is divided into subfamilies: NLRA, NLRB, NLRC and NLRP based on the structure of their N-terminal domain. Several members of the NLR family are involved in activation of inflammasomes while others also drive innate immune responses by the activation of the NF-kB pathway, resulting in the secretion of pro-inflammatory cytokines. In addition, the occurrence of auto-inflammatory diseases has been associated with mutations and single nucleotide polymorphisms (SNPs) in the genes encoding several NLRs.
While innate immune responses are important for controlling microbial infections and maintaining the barrier integrity at mucosal surfaces, a disbalance in the activation of the innate immune system can have deteriorating effects. For example, mutations in protein NOD2 (belonging to the NLRC subfamily) have been associated with inflammatory conditions such as Crohn’s disease, Blau syndrome, arthritis, and other inflammatory conditions. In addition, NLRP1 and NLRP3 have been associated with the occurrence of Type 1 diabetes while NLRP7 has been associated with testicular and endometrial cancers. Interestingly, NOD2 and NLRP6 have also been shown to regulate the response of Toll-like receptors (TLRs) through the control of NF-kB pathway, emphasizing cross-regulatory effects. This research collection aims to delve deeper into the mechanisms by which NLRs regulate inflammatory signalling cascades and further investigate their interaction with other PRRs and the adaptive immune system in the context of various autoinflammatory disorders.
This Research Topic accepts Original Research, Methods, Review and Mini-Review, Hypothesis & Theory, Clinical Trial, Perspective, Case Report, Brief Research Report, General Commentary, and Opinion articles. We welcome manuscripts focusing on, but not limited to, the following sub-topics related to ‘The Role of Nod-Like Receptor (NLR) Family of Proteins in Inflammation’:
• Regulation of inflammation in the mucosal organs by NLR family of proteins.
• The role of NLR family of proteins in the pathogenesis of arthritis.
• Effect of NLR signaling on T and B cell responses.
• Role of NLRs in auto-inflammatory disorders.
• Crosstalk between NLR and other PRRs and its contribution to auto-inflammation.
• Mechanisms by which NLR family of proteins cause mucosal inflammation, arthritis, and cancer.
• Importance of mutations and/or SNPs in NLR-induced inflammation.
Please note: Manuscripts consisting solely of computational analysis of bioinformatics or public genomic or transcriptional databases without validation (independent cohort or in vitro or in vivo biological validation) are outside the scope of this section and are not accepted as part of this research topic. Manuscript dealing with traditional or complementary medicine without a very strong focus on immunological parameters are out of scope for this journal.
While innate immune responses are important for controlling microbial infections and maintaining the barrier integrity at mucosal surfaces, a disbalance in the activation of the innate immune system can have deteriorating effects. For example, mutations in protein NOD2 (belonging to the NLRC subfamily) have been associated with inflammatory conditions such as Crohn’s disease, Blau syndrome, arthritis, and other inflammatory conditions. In addition, NLRP1 and NLRP3 have been associated with the occurrence of Type 1 diabetes while NLRP7 has been associated with testicular and endometrial cancers. Interestingly, NOD2 and NLRP6 have also been shown to regulate the response of Toll-like receptors (TLRs) through the control of NF-kB pathway, emphasizing cross-regulatory effects. This research collection aims to delve deeper into the mechanisms by which NLRs regulate inflammatory signalling cascades and further investigate their interaction with other PRRs and the adaptive immune system in the context of various autoinflammatory disorders.
This Research Topic accepts Original Research, Methods, Review and Mini-Review, Hypothesis & Theory, Clinical Trial, Perspective, Case Report, Brief Research Report, General Commentary, and Opinion articles. We welcome manuscripts focusing on, but not limited to, the following sub-topics related to ‘The Role of Nod-Like Receptor (NLR) Family of Proteins in Inflammation’:
• Regulation of inflammation in the mucosal organs by NLR family of proteins.
• The role of NLR family of proteins in the pathogenesis of arthritis.
• Effect of NLR signaling on T and B cell responses.
• Role of NLRs in auto-inflammatory disorders.
• Crosstalk between NLR and other PRRs and its contribution to auto-inflammation.
• Mechanisms by which NLR family of proteins cause mucosal inflammation, arthritis, and cancer.
• Importance of mutations and/or SNPs in NLR-induced inflammation.
Please note: Manuscripts consisting solely of computational analysis of bioinformatics or public genomic or transcriptional databases without validation (independent cohort or in vitro or in vivo biological validation) are outside the scope of this section and are not accepted as part of this research topic. Manuscript dealing with traditional or complementary medicine without a very strong focus on immunological parameters are out of scope for this journal.
Keywords: NLRs, autoinflammation, inflammasomes, PRRs, arthritis, mucosal immunity
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.
