The field of innate immunity has garnered significant attention due to its critical role in recognizing and responding to microbial threats. Central to this system are Pathogen Recognition Receptors (PRRs), which detect microbial patterns and initiate immune responses. Among these, the Nod-Like Receptor (NLR) family stands out as a group of evolutionarily conserved intracellular PRRs. The NLR family is categorized into subfamilies such as NLRA, NLRB, NLRC, and NLRP, each defined by distinct structural features. Recent studies have highlighted the involvement of NLRs in inflammasome activation and the NF-kB pathway, leading to pro-inflammatory cytokine production. However, mutations and single nucleotide polymorphisms (SNPs) in NLR genes have been linked to various auto-inflammatory diseases, including Crohn’s disease, Blau syndrome, and certain cancers. Despite these advances, the precise mechanisms by which NLRs modulate inflammatory signaling and their interactions with other PRRs remain inadequately understood, necessitating further exploration.

This research topic aims to elucidate the mechanisms by which NLRs regulate inflammatory signaling cascades and to explore their interactions with other PRRs and the adaptive immune system, particularly in the context of auto-inflammatory disorders. By addressing these objectives, the research seeks to answer critical questions about the role of NLRs in inflammation and their potential as therapeutic targets. Hypotheses will be tested regarding the cross-regulatory effects of NLRs and their contribution to disease pathogenesis.

To gather further insights into the complex roles of NLRs in inflammation, we welcome articles addressing, but not limited to, the following themes:
- Regulation of inflammation in mucosal organs by NLR family proteins.
- The role of NLR family 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 proteins cause mucosal inflammation, arthritis, and cancer.
- Importance of mutations and/or SNPs in NLR-induced inflammation.

Please note that manuscripts focusing solely on computational analysis without biological validation or those dealing with traditional medicine without a strong immunological focus are outside the scope of this research topic.

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Frontiers in Immunology

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