The MHC Class-I Chain Related Gene B (MICB) is a protein-coding gene that plays a crucial role in the immune system. It is part of the major histocompatibility complex (MHC) class I family, which is essential for the immune system’s ability to recognize and respond to pathogens. MICB is a stress-inducible ligand that binds to the immunoreceptor NKG2D, which is expressed on natural killer (NK) cells, CD8+ T cells, and γδ T cells . This interaction is vital for the immune system’s ability to detect and eliminate infected or transformed cells.
The recombinant form of MICB is typically produced using molecular cloning techniques. The gene encoding MICB is inserted into an expression vector, which is then introduced into a host cell line, such as E. coli or mammalian cells. The host cells are cultured under conditions that promote the expression of the recombinant protein. After sufficient growth, the cells are lysed, and the recombinant MICB protein is purified using techniques such as affinity chromatography.
For large-scale production, mammalian cell lines are often preferred due to their ability to perform post-translational modifications that are essential for the proper function of MICB. The process involves the following steps:
MICB is involved in several biochemical pathways related to the immune response. It is primarily recognized by the NKG2D receptor on NK cells and certain T cells. This interaction triggers a series of intracellular signaling events that lead to the activation of these immune cells. The binding of MICB to NKG2D can result in the release of cytotoxic granules from NK cells, leading to the lysis of the target cell. Additionally, the interaction can enhance the production of cytokines, which further amplifies the immune response.
MICB expression is upregulated in response to cellular stress, such as infection, transformation, or DNA damage . This upregulation is mediated by various stress-induced signaling pathways, including the DNA damage response pathway. The increased expression of MICB on the cell surface serves as a “kill me” signal to the immune system, marking the stressed cells for destruction.