PE Anti-MICA + MICB antibody [EPR24086-121]

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

MICA and MICB also referred to as Mhc class I polypeptide-related sequence A and B are stress-induced proteins and are known to have a molecular weight of approximately 62 kDa and 70 kDa respectively. They are expressed on the surface of many cell types especially epithelial cells fibroblasts and upon certain cancers. These proteins are encoded within the MHC class I region yet unlike classic MHC class I molecules they do not associate with beta-2-microglobulin and they do not present antigens to T cells. Instead MICA and MICB can activate immune responses by engaging the NKG2D receptor on natural killer (NK) cells CD8+ T cells and gamma-delta T cells.

Biological function summary

MICA and MICB contribute to the immune surveillance system by marking stressed or transformed cells for destruction. These proteins are not part of a complex but are known ligands for the NKG2D receptor. Their interaction with NKG2D triggers the cytotoxic activity of NK cells and CD8+ T cells enhancing the destruction of cancerous or infected cells. Especially interesting is their role in tumor immunology where they serve as a danger signal to the immune system pointing NK cells toward tumor cells that would otherwise evade detection.

Pathways

The role of MICA and MICB centers around the immune response and cell stress pathways. One important pathway is the stress-induced signal transduction which upregulates these proteins in response to cellular stress such as heat shock. They fit into the immune surveillance pathway interacting with proteins like the NKG2D receptor and other signaling molecules that modulate immune cell activation. The pathway emphasizes the removal of damaged or abnormal cells and this interaction orchestrates timely immune responses.

MICA and MICB have associations with certain cancers like liver and colorectal cancers where they become over-expressed and shed from tumor cells to escape immune detection. Additionally their presence links to autoimmune diseases such as rheumatoid arthritis where the immune system attacks the body's own cells unjustly. The shedding of MICA/MICB from tumor cells involves enzymes like metalloproteinases affecting the engagement of NKG2D and complicating the immune response to cancerous cells.