CDC11c+ mononuclear phagocytes expressing high levels of Cx3cr1 (chemokine (C-X3-C motif) receptor 1) have been found to traffic bacteria from the gut to mesenteric lymph nodes (MLNs) where T-cell responses and IgA production are induced. 
 CX3CR1-STOP-DTR (Cx3cr1-loxP-STOP-loxP-DTR-IRES-YFP) knock-in mice have a loxP-flanked STOP cassette upstream of the diptheria toxin receptor (Hbegf formerly DTR)-coding region, all knocked into exon 1 of the mouse Cx3cr1 locus. Although YFP is incorporated in the knock-in construct, YFP expression is not observed. These mice allow Cre-inducible depletion of cells upon administration of diphtheria toxin.
 For example, expression of CD11c-Cre (e.g. through crosses with Stock No. <a href="https://www.jax.org/strain/008068">008068</a>) excises the STOP cassette, allowing for DTR expression and selective depletion of CD11c+CX3CR1hi cells upon administration of diphtheria toxin, with no effect on CD11c+ CX3CR1int or CD11c+CD103+cells. When mice are orally infected with non-invasive Salmonella after diptheria-toxin-mediated depletion of the CX3CR1hi mononuclear cells, there is a marked reduction in the number of bacteria reaching the mesenteric lymph nodes.

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CX3CR1-STOP-DTR (Cx3cr1-loxP-STOP-loxP-DTR-IRES-YFP) knock-in mice have a loxP-flanked STOP cassette upstream of the diptheria toxin receptor (Hbegf formerly DTR)-coding region, all knocked into exon 1 of the mouse Cx3cr1 locus. Although YFP is incorporated in the knock-in construct, YFP expression is not observed. These mice allow Cre-inducible depletion of cells upon administration of diphtheria toxin.

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B6N.129P2-Cx3cr1<tm3(Hbegf)Litt>/J Frozen Embryo