Table 2.

Intrapancreatic DC, macrophages, and B cells in NOD mice

	Phenotype	Demonstrated or proposed role/function	Concomitant events inside pancreas
DC	XCR1+ CD103+ Batf3+	Increase in numbers beginning at 3 weeks of age	Insulin-reactive CD4+ T cells evident inside the pancreas and around the islets
		CD103+ DC cross present class I MHC epitopes to CD8+ T cells, and Batf3 is necessary for this function	Insulin-reactive T cells are in tight physical contact with the CD103+ DC, which exhibit an interferon-inducible gene expression signature
	Batf3-deficient NOD mice		XCR1+ CD103+ DC were absent in the islets, transgenic mice remained diabetes free and without evidence of islet-reactive T cells; poor priming of diabetogenic CD4 and CD8 T-cell responses
Macrophages	Derive from hematopoietic progenitors, slow replicating, not replaced by circulating monocytic precursors	Filopodia extend into the microvasculature	Deletion of islet-resident macrophages eliminated T-cell entry into islets and reduced diabetes incidence in NOD mice
	Exhibit a proinflammatory gene signature	Sense blood-borne molecules
	Resemble lung “barrier macrophages” with high lysosomal content and activity	Physically adjacent to β-cells and take up insulin-containing crinosomes