Monday, March 12, 2012

Delicate Balances

The biological world are full of majins. Please refer to our previous post for the definition of the word.
Like I said the biological world are full of majins; all interconnected to one another in the strangest of ways. Autoimmunity is a subject that thrills me. For those of you are unfamiliar to the concept, it's quite simply put. It's when your immune system- that which guards you from bacteria, viruses and worms- loses its ability to distinguish friend from foe and goes on a wild rampage attacking the body cells and causing tissue damage in the long run. Imagine a situation of friendly fire and you get the idea.Examples range from multiple sclerosis, systemic lupus, Graves Disease and Type I diabetes. So to give you a very, very general outline, it's like this: there are two types of cells called the B and T cells which mature in the bone marrow and the thymus respectively. The T-cells can potentially detect millions of different antigens , but they need help. Cells called dendritic cells (a part of the antigen-presenting cell milleu) can process antigens and "present" them to the T-cells for analysis. If the T-cell recognizes the antigen, it makes clones of itself and then it interacts with B-cells to produce antibodies via plasma cells. So APC present the foreign antigens to T-cells, T-cells activated, they interact with B cells to make the B-cells differentiate into plasma cells that in turn produce antibodies.
These antibodies then take care of the infection by blocking their adhering to the cell surfaces, "coats" them and targets them for destruction via phagocytosis (cell- eating!).
With me so far?
Right.
Balance 4
Balance 4 by Darkr; CC BY-NC 2.0
Now there are these cell signaling protein molecules called cytokines that are produced and that also facilitate the above processes. There are loads of them: IFN-Gamma, Interleukin-1 (IL-1), IL-6,IL-17,IL-22, TGF-Beta and so on. Now some of them cause inflammation and some of them ameliorate them.
The interesting part now comes up...The TGF-Beta inhibits the activation of the APC, presentation of antigen to T-cell is stopped and thus T-cell activation is inhibited and so further immune responses are stopped. This is very useful if the T-cell recognizes an antigen from the body and starts mounting an immune response ("the friendly fire" analogy that leads to autoimmunity). It also gives way to the development of a subset of T-regulator cells that step in to stop further reactions against self antigens. So that's done neatly right?

Strangely enough, the very same cytokine, TGF-Beta, plays a role in developing another subset of T-cells called Th-17 that produce pro-inflammatory cytokines.
Thus an anti-inflammatory cytokine TGF-Beta in the presence of other cytokines can drive the development of pro-inflammatory cytokine- producing T-cell subsets, that might invariably contribute to autoimmunity! The solution and problem are connected through the same elaborate network. Majin!

1 comment:

Vyaas said...

"The TGF-Beta inhibits the activation of the APC, presentation of antigen to T-cell is stopped and thus T-cell activation is inhibited and so further immune responses are stopped. This is very useful if the T-cell recognizes an antigen from the body and starts mounting an immune response ("the friendly fire" analogy that leads to autoimmunity)."

Sounds like TGF-Beta is a double edged sword. What if the antigen is not from the body?

Reading that reminds me why I could never pursue medicine. The sheer amount of terminology is enough to inflict multiple cardiac arrests AND a brain haemorrhage.
But of course, I'm sure the nomenclature is well laid out and one, with enough industry can find their way through the caves and crevices of jargon. And I'm thankful that such people exist, such as yourself.