**2.2 The alternative pathway**

NF-κB2 p100/RelB complexes are inactive in cytoplasm. Signaling in LTβR, CD40, BR3 activate kinase NIK [26] which in turn activate IKKα complex that phosphorylate C terminal residue in NF-κB2 p100 which leads to ubiquitination and proteasomal processing to NF-κB2 p52 and translocate to nucleus to target gene expression [27]. The pathway regulates important aspects of immune functions, including lymphoid organ development, the cross-priming function of dendritic cells, B cell survival and germination center reactions, generation and maintenance of effector and memory t cells, antiviral innate immunity [28]. The pathway is responsible for inflammatory disease, kidney inflammation, metabolic inflammation and central nervous system inflammation [29]. Recent evidence suggests that NF-κB also has a role in regulating the activation of inflammasomes. Dysregulated NF-κB activation is a hallmark of chronic inflammatory diseases. Therefore, a better understanding of the mechanism that

*Perturbation of Cellular Redox Status: Role of Nrf2, a Master Regulator of Cellular Redox DOI: http://dx.doi.org/10.5772/intechopen.102319*

underlies NF-κB activation and pro-inflammatory function is of great significance for therapeutic strategies in the treatment of inflammatory diseases.
