In a step toward developing drugs against autoimmune disease, George Washington University researchers have identified proteins called transcription factors as a “vital component” in determining the function of immune T cells.
GWU’s Weiqun Peng, an associate professor of physics, and PhD candidate Zhouhao Zeng collaborated with University of Iowa immunologists to determine what gives rise to different types of T cells. Healthy people have CD4, or helper T cells, and CD8, or killer T cells, in a certain range of ratios, but people with autoimmune disease or viral infections have them in skewed proportions.
“If something goes wrong in the CD4/CD8 mix, our ability to fight off infections and diseases is compromised,” Zeng said, as reported by GW Today.
Transcription factors affect a cell’s transcription patterns, regulating gene expression. In the case of T cells, Peng’s research shows that the transcription factors Tcf1 and Lef1 activate genes in a pattern that preserve killer T cell identity. If this transcription pattern is disrupted, the cells become more like helper T cells, GW Today reported. This previously unknown function of Tcf1 and Lef1 represents a potential drug target for autoimmune disease.
“But if biomedical scientists can develop strategies to turn on/off the T-cell differentiation pathway, we might be able to make drugs that hit the molecular target" and reinforce our immune systems,” Zeng said.
Earlier this year, St. Jude researchers discovered that the oncogene c-Myc can control asymmetric division in T cells, which causes them to divide not into two identical effector or memory T cells, but into one of each. Changing the concentration of the oncogene can influence the levels of each type of cell, which can potentially lead to improved cancer treatments.