Autoimmune diseases such as multiple sclerosis and rheumatoid arthritis arise when immune cells turn overactive and target the body’s healthy tissues. Scientists at the Georgia Institute of Technology have found a method the body utilizes to remove the T cells that trigger autoimmune disorders—a result they consider can motivate new treatments for these diseases.
The method of destroying damaging immune cells begins with thymocytes—the antecedent cells which ultimately grow into T cells. The scientists found a mechanism through which the body identifies strangely aggressive thymocytes and evokes them to commit suicide prior to they develop into T cells.
They explained that process as a “two-handed handshake.” After thymocytes structure in the bone marrow, the TCRs (T-cell receptors) on their surface are checked by the body to assure they are capable of identifying self-antigens, which recognize the cells of the body. Then they process the TCRs through a 2nd test to ascertain they do not react excessively to self-antigens. The cell that doesn’t pass either test is shoved toward suicide.
The scientists examined the cell interactions that result in destruction of thymocytes and found a signaling loop. The TCR is signaled by the self-antigen from a cell. If the TCR reacts excessively, the thymocyte stimulates CD8, a kind of lever that informs the thymocyte to suicide prior to it develops into a T cell.
Comprehending the selection mechanisms that prevent the immune cells from harming healthy tissue, while battling cancer and infection, can someday result in the advancement of new immune-regulating treatments.
Likewise, bacteria that dwell in the human gut might stimulate autoimmune reactions by generating human-like proteins that imitate a naturally existing and vital cell protein. Scientists at Queen’s University Belfast mention that autoimmune disorder patients—like rheumatoid arthritis, ulcerative colitis, and multiple sclerosis—have more-than-standard levels of a “mimic protein” generated by Bacteroides fragilis—a gut microbiome member in people.