Elizaveta Shpilevaia Student # 1006640The purpose of the study collected by Mantsuno et. al (2002) was to reveal if certain pro-inflammatory cytokines, TNF-alfa and IL-6, were truly the primary stimulators of synovium destruction. A closer inspection of these secreted proteins with a specific effect on the cell-to-cell interactions (Zhang and Jianxiong 2007) can be helpful in the understanding of Rheumatoid Arthritis pathogenesis and how it affects the immune system. The experiment was carried out using SCID (severe combined immunodeficiency) mice (Mantsuno et. al 2002). To gather the research, scientists injected the rodents with synovia samples taken from RA patients (Mantsuno et.
al 2002). After, a four-week trial started by administration of the anti-TNF-a mAbs into the implanted tissue of 16 mice, and human TNF-a and IL-6 into 24 mice (Mantsuno et. al 2002). It suggests that SCID mice are considered a reliable model for biological agent analysis and have a similar physiology and anatomy as humankind.
Scientists also aimed to test if TNF- blockage was preventing the abrasion of bones based on their research results (Mantsuno et. al 2002). While the anti-TNF treatment decreased the number of inflammatory cells and the affected tissue, there were no significant changes in TNF-a and IL-6 treated groups; TNF- alpha administration only increased cytokines production without any damage caused (Mantsuno et. al 2002). It brings the idea that there might be other pathological ways involved in the destruction of the joint, and TNF not being primary. One may say that a longer trial, as well as a bigger test group, could possibly yield different and more reliable results.
In conclusion, the study provides evidence that TNF-alpha is a major factor controlling the inflammation in the RA but not leading to any destruction. It shows that RA pathogenesis is a much more complex matter involving various pathways yet to be discovered.