Frequently, autoimmune disorders come in combinations. For example, a subset of human patients with type 1 diabetes (T1D) develop autoimmune polyglandular syndrome (APS) that depending on type (APS types 1-4) involves other tissues such as thyroid, adrenal, submandibular, and lacrimal glands.
New study published in Journal of Immunology and conducted in autoimmune-prone mouse strain, NOD, showed that presence of microbiota modifies immunopathology in a tissue-specific manner.
For instance, female NOD mice devoid of microbiota (GF NOD mice) showed reduced pathology in salivary glands (sialitis) but as expected no change or worsening of pathology in pancreas (insulitis).
Similarly, MyD88 deficiency completely abolished sialitis in both WT and GF female mice but it couldn't rescue insulitis phenotype on GF background (as reported prevously).
In summary, this short study suggests that microbiota → MyD88 pathways directly influence development of sialitis, while for insulitis (and diabetes development) microbiota/MyD88 pathways diverge.
David Usharauli
For instance, female NOD mice devoid of microbiota (GF NOD mice) showed reduced pathology in salivary glands (sialitis) but as expected no change or worsening of pathology in pancreas (insulitis).
Similarly, MyD88 deficiency completely abolished sialitis in both WT and GF female mice but it couldn't rescue insulitis phenotype on GF background (as reported prevously).
In summary, this short study suggests that microbiota → MyD88 pathways directly influence development of sialitis, while for insulitis (and diabetes development) microbiota/MyD88 pathways diverge.
David Usharauli
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