Immune Function and Drug Discovery: The Genetics of Immunity

Author(s): Dr. Ben Stokes

An organism's defense mechanism against pathogenic stress includes the immune system as an essential component. Increased susceptibility to infections, increased onset and progression of autoimmune diseases, and the onset of neoplastic diseases are all symptoms of age-associated immune dysfunction, which is also known as "immune senescence." In terms of the phenotypic and functional defects in the immune system of various organisms, including humans, extensive research has produced consensus over the years. It has been demonstrated that immune decline is caused by age-related changes like thymic involution, skewing of the T cell repertoire, decreased capacity to activate naive T cells, and diminished capacity to generate robust memory responses. In addition, identifying the signaling pathways that interact with immune senescence and influence it has been made possible by comprehending the molecular mechanisms that are responsible for the development of proteotoxic stress, the DNA damage response, the modulation of the ubiquitin proteasome pathway, and the regulation of transcription factor NFB activation in immune decline.