These are common variants linked to autoimmune conditions in population studies. They are not diagnoses or personal risk scores, and the largest common genetic contributor of all, the HLA region, is not typed here.

The Biology

Autoimmune conditions arise when the immune system treats the body's own tissue as a threat. Their genetics are strongly polygenic: the HLA class II genes contribute the largest common effect, and beyond HLA a long tail of common variants in immune-signaling genes each add a small amount. The three variants here are well-studied members of that non-HLA tail.

As with the rest of this catalog, these are population associations, not readouts of your own immune biology. Typical odds ratios sit near 1.2 to 1.5 in the cohorts that reported them. As a plain anchor, an odds ratio of 1.3 means people with the higher-association genotype had about 30 percent greater odds of the diagnosis than people without it in those studies. That is a relative comparison between groups, not a fixed change to any one person's chance, and it stays small in absolute terms when the baseline risk is low. The estimates are drawn predominantly from European-ancestry studies, and Varia does not infer your ancestry from your file.

What Varia Analyzes

Three non-HLA loci, each among the most replicated common autoimmune-susceptibility variants:

PTPN22 rs2476601 (the R620W variant), associated with rheumatoid arthritis, type 1 diabetes, and several other autoimmune conditions.

STAT4 rs7574865, associated with rheumatoid arthritis and systemic lupus erythematosus.

ITGAM rs1143679, associated with systemic lupus erythematosus.

Each is reported with its genotype, the strength of the underlying evidence, and the leading citations. Where a genotype carries no copies of the associated allele, that is stated plainly rather than dressed up as a result.

How to read these findings

A higher-association genotype here is a small, partial piece of population context. Most people who carry these common risk alleles never develop the associated condition, the effect is not deterministic, and the single largest genetic contributor for these diseases, HLA, is not even in view.

The drivers these findings leave out are substantial: HLA type, other non-HLA genes, infections and environmental exposures, sex, and family history. A finding on this page is not a diagnosis, not a reason to start or stop any treatment, and not a substitute for evaluation by a clinician if you have symptoms or a family history that concerns you.