Branching from that broader susceptibility are a number of other genes and genetic markers that contribute to specific diseases, such as ankylosing spondylitis, systemic lupus erythematosus (SLE) or Type 1 diabetes.

Researchers interested in autoimmunity are looking into the HLA (human leukocyte antigen) complex to learn more about what may cause JIA. This cluster of genes, which reside on chromosome 6, is believed to play a significant role in fighting infection, as well as in the development of autoimmunity. In addition to the genes themselves, there are also related proteins that help the body’s immune system distinguish between its own cells and nasty invaders such as viruses.

We’re still in the early days of understanding what genetic markers may mean for our health, but researchers are starting to associate certain genes on the HLA complex with an increased risk of specific diagnoses. Testing positive for HLA-B27 is associated with a higher risk of developing one of the spondyloarthropathies. Other genes, such as HLA-DR1 and HLA-DR4, appear to be linked with children who have rheumatoid factor-positive polyarthritis.

HLA isn’t the only autoimmune region under the genetic microscope. In recent years, researchers have turned their sights on the PTPN22 variation, located on another chromosome, which they believe is associated with adult rheumatoid arthritis, juvenile rheumatoid arthritis, lupus and autoimmune thyroid disease.

So what does this new knowledge mean for you? Important genetic tests are being developed now, but their results may still not tell us what we need to know. Insightful in some cases, they may only provide a piece of the puzzle. Take the HLA-B27 test: The overwhelming majority of those diagnosed with ankylosing spondylitis, an arthritis that primarily affects the spine, will test positive for HLA-B27, particularly if they are Caucasian.

But individuals can carry HLA-B27 without developing any related arthritis of the spine.

By the same token, genes aren’t singularly bad. For every gene or genetic marker, such as a protein, that might nudge your child a little closer to developing an autoimmune condition, there are believed to be another set of genetic components that step in to slow or halt the process.

Furthermore, genes are likely only part of a two-step process. As with many other diseases, such as cancer, environmental triggers are believed to play a role. Your child may, to a greater or lesser degree, have a genetic profile that boosts her risk of developing arthritis, but having a particular genetic makeup, when coupled with certain outside influences, may tip the balance.