Washington D.C: In a new study, scientists have explored the relationship between fever and cancer incidence.
The recurring patterns in patient accounts suggest the existence of an inverse relationship between the history of infectious fever and cancer risk which are documented throughout decades of medical literature.
However, evidence supporting this correlation continues to be primarily anecdotal.
Drawing upon previous research and experimental data, the authors argue that repeated exposure to fever enhances the ability of gd T cells to detect cellular abnormalities and to foster inhospitable environments that destroy malignant cells.
This paper is the first to acknowledge the role that gd T cells may play as participants in this inverse relationship.
Infectious fever is the defensive and adaptive reaction that occurs when an organism’s immune system comes into contact with exogenous pyrogens, or pathogen-associated molecular pattern (PAMP). Upon recognition of these exogenous pyrogens, endogenous mediators–also known as endogenous pyrogens–engage the febrile system.
The authors further elaborate on the function of endogenous mediators, like cytokines.
“In short, endogenous mediators of fever redirect metabolic substrates and energy to the immune system during fever. This markedly enhances the frequency of a vast range of immune effectors, including lymphocytes expressing gd heterodimer receptors, which possess a potent anti-infectious and antitumor competence,” wrote authors.
Exposure to infection significantly expands the quantity of gd T cells. During infection, blood Vg9Vd2 T cells can increase in number until they constitute 60 percent of the total amount of lymphocytes.
While previous research and current cancer immunotherapy practices predominately focus on alpha/beta (ab) T cells, analysis of the interaction between fever and gd T cells may generate further inquiry into the larger impact and the clinical benefits of this relationship.
The full findings appeared in the journal- Quarterly Review of Biology.