Mice are one of the most commonly used vertebrates in medical research, and their role as an animal model for humans could be called invaluable. However, in an early release paper from Science, researchers point out a case where mice are not ideal models for a protein deficiency that predisposes patients to suffer from specific infections in their first ten or so years of life.
MyD88 (Myeloid Differentiation primary response gene 88) is a protein that mediates the interactions of Toll-like receptors and interleukin-1 receptors. The two receptors are significant participants in immunity, as they are both involved in recognizing invading microbes, inducing fevers, and activating cells of the immune system.
A deficiency in MyD88 is detrimental to children because it interferes with important signaling processes that are necessary for fighting specific strains of bacteria. As people grow older, the consequences of MyD88 deficiency lessen as the immune system compensates for this flaw. Although MyD88 deficiency can be overcome with age, it is still dangerous, as most affected children would not survive without the help of antibiotics. Out of the nine children investigated by the researchers, three died before their first birthday.
One issue that could hinder research in MyD88 is that mice and humans react differently to its deficiency. At the immunological level, mice and humans are similar, meaning that comparable signaling processes are disrupted. However, in terms of infectious symptoms, there are huge differences between humans and mice that lack MyD88.
Humans with MpD88 deficiencywere predisposed to be susceptible to Streptococcus pneumonia (pneumonia, meningitis, brain abscess, etc.), Staphylococcus aureus (pneumonia, toxic shock syndrome, meningitis, boils, etc.), and Pseudomonas aeruginosa (urinary tract infections, pneumonia, dermatitis, etc.). But, in addition to the above, mice that lacked this gene were vulnerable to nearly all the pathogens that the researchers tested, which included 19 bacteria, seven viruses, four fungi, and five parasites.
Since mice and humans respond differentlyto MyD88 deficiency, the mostpopular animal model would not be an ideal choice for this line of medical research. That means researchers will be limited to alternatives such as cell culture techniques or possibly other animal models.
Science, 2008. DOI: 10.1126/science.1158298