Although it is no surprise that
most illnesses will affect several areas of a person’s body, it never ceases to
amaze us how many illnesses that appear so dissimilar on the face of it have a
shared underlying mechanism. A perfect example of that comes from a recent
study, which considered the role of the BACH2 gene in autoimmune diseases.
The study, which was carried out by National Cancer
Institute (NCI) and the National Institute of Arthritis and Musculoskeletal and
Skin Diseases (NIAMS), was recently published in Nature. The key findings from this animal study indicated that mice
whose BACH2 gene had been removed, exhibited inflammatory cells and died within
the first months of life. However, when the researchers carried out so-called
gene therapy and reinserted the same gene, then the mice’s ability to produce
regulatory cells was restored, and they recovered. The findings further
suggested that the role of the BACH2 gene was so vital because it acted as a
regulator between CD4+T cells and regulatory T-cells. Based on this, the
researchers urged for more studies to consider the role of the BACH2 gene in
humans and its potential implications for future treatments.
The findings from this study appear rather robust and are
in line with current knowledge as well as previous research. It is commonly
known that the immune system has various cell types, which must act in unison
to maintain a healthy balance. This becomes more complex when it comes to white
CD4+T cells, as they can activate or constrain immune responses. In allergic
and autoimmune disease, such as type I diabetes, multiple sclerosis, asthma,
Crohn's disease, and celiac disease, the immune responses become uncontrolled
which in turn leads to the body’s own cell and tissues being attacked by their
immune system. In terms of research, the results of the current study clearly
extend on findings from genome-wide association studies. Specifically, past
studies from diverse populations have suggested that individuals who develop
allergic or autoimmune diseases often have a compromised immune system as well
as minor variations in the BACH2 gene.
We agree with the researchers that more studies need to be
done to fully understand the role of BACH2. Perhaps the first approach would be
to consider conducting human studies. If these prove fruitful, then it would be
valuable to see whether there are any current treatments for other illnesses
that could affect this process. Although it may be controversial, we are
inclined to say that the research should be taken a step further to consider
whether there is an underlying process that affects which CD4+T cells become
the cells that activate or constrain immune responses.
There is a long way until we can see the full implications
of these findings. Nevertheless, they are one step in the right direction. More information can be accessed here.