How does our immune system change as we age?
It’s been known for a while that as we age we become less effective at fighting off infections from viruses and other pathogens, however the precise reason for this immunological change is not clear. By compiling multiple studies from across the globe researchers are homing in on some of the potential mechanisms for what is being called “immunosenescence” or “immunopause” and cytomegalovirus (CMV) is being hypothesized to play a major contributing role.
CMV, a member of the herpesviridae virus family, is purported to infect between 60% and 80% of the human population (~100% in developing countries) and remains in the body for life.
The persistence of CMV in the body has major implications for both young and aging individuals. Because of its chronic presence in the body, it is continually targeted by CD8+ T-cells, the cells in the body charged with finding and helping to destroy virally infected cells. Usually, upon expelling a viral infection from the body, T-cell populations will go into a dormant state by forming memory T-cells. Memory T-cells stick around and “remember” what viruses the body has been exposed to, so that you can mount an immune response easier upon re-infection.
The problem comes from the fact that CMV is a chronic viral infection, meaning it is never fully cleared from the body. T-cells are continually recognizing CMV antigens, and are continually differentiating into CMV-specific memory T-cells. These CMV-specific memory T-cells “crowd out” T-cells responsible for recognizing other pathogens and decrease the overall effectiveness of the T-cell immune response.
Whether or not CMV is the primary cause of immunological aging, or simply the most obvious causative agent of this “crowding out” process is unknown as of yet.
Further studies are needed to expand on the effects of other known immunological aging defects, such as chronic inflammation and a variety of other common disease states.
Gram-negative Bacteria have just entered the body
Macrophages circulate throughout the body looking for things that shouldn’t be in the body, see the bacteria and call
And the Neutrophils come running, ready to kill the bacteria!
The Neutrophils then phagocytose the bacteria
And die :(
Neurons communicate with one another by releasing chemicals, such as dopamine, from pouches called vesicles. The vesicles, seen here in a fibroblast cell, have a geodesic outer coating that eventually pops through the side of the cell and releases its chemical message to be detected by the cell’s neighbors.
“The white elements in the picture are the axons from the olfactory sensory cells located at the front of the brain. They carry information about different molecular components of odors. The red parts are the synaptic terminals that are located inside of these axons and these terminals are the cellular sites at which neural information (i.e., action potentials or electric signals) are converted into a chemical signal which then moves over to another neuron and activates it.”
Department of Physiology & Biophysics
- Oliver Braubach
A comparative anatomy of the hand from The Natural History of the Ordinary Cetacea, or Whales (1837), by Robert Hamilton. Diagrams C and D show the bony structures in the flippers of a dugong and a bowhead whale, respectively. Diagram E shows a human arm for comparison.
That awkward moment when your eyes can’t decide if it wants to use cones or rods.
The retina in your eyes contains two types of photoreceptors: