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Table 2

Intrapancreatic DC, macrophages, and B cells in NOD mice

PhenotypeDemonstrated or proposed role/functionConcomitant 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  
PhenotypeDemonstrated or proposed role/functionConcomitant 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  
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