Autoantibodies
You want none: their appearance is the first visible sign that the attack has begun.
In depth
Antibodies against the beta cell's own proteins — GAD, IA-2, ZnT8 and insulin itself. Seroconversion marks the disease process years before blood sugar ever moves, which is why type 1 is diagnosed late and why prevention has to start early.
What drives it
Islet inflammation increases it.
The siege leaves fingerprints. Verbatim: 'Type 1 diabetes-related autoantibodies were first described in the early 1970s... including insulin autoantibodies (IAA) and autoantibodies to glutamic acid decarboxylase (GAD), an aborted tyrosine phosphatase (islet antibody-2 or IA2), and the zinc transporter (ZnT8), all components of beta cells' (NBK604182). autoantibodies mark the process; they are not themselves proven to be the destroying agent - the effector arm is cellular.
Coxsackievirus B3 increases it.
Verbatim: 'Prospective epidemiological studies have strongly associated the persistence of enteroviruses, especially coxsackievirus B (CVB), with the appearance of islet autoantibodies and an increased risk of T1DM' (doi 10.1038/s41574-022-00688-1). The association is 'linked to autoimmune initiation (ie, islet autoantibody seroconversion) rather than to clinical progression'. initiation only - it does not predict how fast an individual progresses after seroconversion. doi 10.1038/s41574-022-00688-1
What it drives
It increases Type 1 diabetes.
Verbatim: 'Seroconversion is an important marker of the type 1 diabetes disease process' (NBK604182). ENDIT recruited on exactly this basis - '552 relatives with confirmed islet cell antibody (ICA) levels of 20 JDF units or more'. seroconversion predicts but does not guarantee; progression rate varies, and the number of antibodies detected changes the risk.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.