Monoclonal Antibodies are obtained from cells derived by cell division from a single ancestral cell. Thereby, monoclonal antibodies have the same sequence, structure and bioactivity. Nowadays, monoclonal antibodies are a class of antibodies expressed by hybridoma derived from a single clone and can be grown stably and indefinitely. Monoclonal antibodies can recognize and bind to specific antigens as design. They work in different ways depending on the protein that they target.
The first monoclonal antibodies were obtained entirely from mouse cells. Thus, the biggest problem is that these monoclonal antibodies will be recognized by human immune system as foreign and will induce an immune response against them. This means that the antibodies may only work effectively the first time they are provided and they will be cleared by body’s immune system when they are provided again.
In addition, fragments of antibodies are used to replace the whole ones. Smaller pieces may reach a tumor easier with higher efficiency. Till now, many different monoclonal antibodies are already available to treat cancer.
How monoclonal antibodies are produced
Monoclonal antibodies are obtained through a certain cell called hybridoma which is formed by B-Lymphocyte and myeloma. The hybridoma cells combine the characteristics of B-Lymphocyte and myeloma. B-Lymphocyte is able to produce antibodies and tumor cell myeloma is able to grow indefinitely. In this case, hybridoma cells grow faster than normal cells and they are stable, and one type of hybridoma secretes one certain specific antibodies. For example, if the mice are injected with a certain antigen, some B-Lymphocytes of the mice will secrete those specific antigen antibodies. Fusion with myeloma and forming the hybridoma, monoclonal antibodies against the specific antigen are obtained indefinitely. For the screening of hybridoma, the myeloma cells need to be lack of the ability to synthesize hypoxanthine-guanine-phosphoribosyl transferase (HGPRT) enzyme. HGPRT helps cells to synthesize purines using an extracellular source of hypoxanthine. When exposed to aminopterin, this type of myeloma is unable to use other pathway and fully depends on HGPRT for their survival. In this case, unfused myeloma cells can’t survival for the lack HGPRT. In addition, unfused normal B cells can’t survival for a limited life-span. At last, only hybridoma cells can survival for HGPRT provided by B cells and the partner of myeloma to divide.