| | Strain | Results | Refs |
| | NOD/Lt | (i) Increased TLR1, TLR2, TLR4, TLR9, and MyD88 expression at pre-clinical and clinical disease stages
(ii) Chloroquine reduced sialadenitis and TLR1, TLR2, TLR3, TLR4, and TLR9 expression in SMG tissue | [24] | | NOD/Lt | (i) Lymphocytes expressing TLR9 are present in SMG tissue
(ii) PBMCs coexpressing TLR9 and p-p38 MAPK are elevated in NOD/Lt animals at 5, 8, and 10 weeks of age compared to BALB/c controls | [29] | | NOD | (i) TLR9 ligation increased salivation | [30] | | C57BL/6.NOD-Aec1Aec2 | (i) TLR3, TLR7, and downstream signaling intermediates are elevated at pre-clinical disease time point in SMG tissue | [33] | | NOD.B10 | (i) MyD88-deficient females are protected against local and systemic pSS manifestations | [36] | | NZB/WF1 | (i) TLR3 agonism with poly(I:C) increased IFNβ, Mx-1, PRKR, IF144, IL-6, TNFα, and CCL5 in salivary tissue and resulted in loss of salivation | [39] | | NZB/WF1 | (i) Poly(I:C) upregulated CCL2, CCL3, CCL4, CCL7, CCL11, CCL12, CXCL10, and Cxcl13 in SMG tissue
(ii) Poly(I:C) induced robust and accelerated salivary inflammation and diminished saliva production | [40] | | C57BL/6 | (i) Poly(I:C) treatment caused reduced salivation and increased IL-6, IL-10, and IL-27p28 in SMG tissue | [41] | | C57BL/6 | (i) Poly(I:C) induced upregulation of chemokines in lacrimal tissue, dacryoadenitis, and reduced tear production | [43] | | C57BL/6 | (i) LPS treatment induced sialadenitis, increased TNFα, IFNβ, IFNγ, and IL-6 in SMG tissue, and caused hyposalivation | [42] | | C57BL/6 | (i) Flagellin caused salivary inflammation, increased inflammatory cytokines and chemokines in sera, and autoantibodies | [44] |
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