THE BTK OVEREXPRESSION IN B CELLS POSSIBLY SYNERGIZES WITH ANOTHER MOLECULE/GENE/MOLECULAR NETWORK/GENETIC NETWORK TO HAVE THE SAME PHENOTYPE AS THE BTK DEFICIENCY- A HYPOTHESIS

Abstract

The cross-linking of the B cell receptors (BCRs) located on the surface of the B cell by an appropriate antigen provides the stimulus to initiate a biochemical cascade that culminates in the production of mature B cells, memory B cells and Immunoglobulin (Ig)-secreting plasma cells. Bruton's Tyrosine Kinase (BTK) is an important non-receptor cytoplasmic molecule that takes part in this biochemical cascade. Interestingly the two most important indicators of the occurrence of BTK deciency-driven genetic disorder X-linked agammaglobulinemia (XLA) in an individual are the absence of mature B cells and very low serum Ig levels. This fact prompted me to probe the role and or function of the BTK molecule in the B cell to greater depth. And for this purpose I reviewed/analyzed the literature not only related to Chronic Lymphocytic Leukemia (CLL) but also related to the treatment of CLL with Ibrutinib. The reason for choosing CLL disease model is that Ibrutinib is a BTK inhibitor which has shown promising results in treating CLL. In the process I derive an important hypothesis associating the BTK expression level with particular phenotype. This hypothesis fully explains the response of a CLL patient to Ibrutinib treatment