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For more than a decade, the nuclear factor kappa-B (NFκB) family and their signaling pathways have proved crucial to the immune system's functioning. According to research, this factor is implicated in almost every immune system event, including immune cell development and function, activation, and pathogen-activated cell death. A considerable body of evidence suggests the idea that, in addition to being a possible transcription factor, it plays a very significant role in the establishment of inflammation-associated immunological responses in host cells. Inflammation is a cascade of events that involve vasodilation and immune cell migration to the site of infection in order to defend the host. However, if dysregulation occurs, it may lead to the emergence of chronic inflammatory illnesses. When immune cells migrate to an inflamed area NFκB activation occurs, which causes release of pro-inflammatory cytokines and development of inflammatory response. Furthermore, this complex transcription factor activation takes part in several innate and adaptive immunity-related cellular processes, including immune cell proliferation and differentiation. Grasp the relationship between the immune system and inflammation requires a thorough understanding of NFκB's capabilities. This review explores the role of NFκB activity as a key inflammatory mediator in various malignancies and auto-inflammatory diseases. We have shed light on how NFκB regulates inflammatory responses by producing cytokines and chemokines and directing the transcription of inflammatory molecules involved in both innate as well as adaptive immunity.
Mukherjee et al. (Mon,) studied this question.