example klrb1 antibodies  (R&D Systems)

Journal: Nature communications

Article Title: Innate lymphocyte-induced CXCR3B-mediated melanocyte apoptosis is a potential initiator of T-cell autoreactivity in vitiligo.

doi: 10.1038/s41467-019-09963-8

Figure Lengend Snippet: Fig. 1 Increased detection of innate immune cells in non-lesional skin of vitiligo patients. Immunofluorescence depicting NK cells (a, b, c) and ILC1 (d, e) in the skin and in the peripheral blood (f, g) of vitiligo patients (n = 6) and healthy controls (n = 5). Number of yellow-immunoreactive CD56 + GranzymeB+ NK cells and their semi-quantification in non-lesional (NL) and lesional (L) skin of vitiligo patient compared to healthy skin are shown in a and the number of CD56+IFNγ+NK in b. The presence of NK cells (CD3-CD56+) was confirmed by immunohistochemistry showing cells to be located just under the epidermis of non-lesional (NL) skin (c bottom left and magnified in 1–4) but less in lesional (L) (c top) or healthy skin (c top right). d Depicts Tbet+CD161 +ILCs in the skin and their quantification. In the peripheral blood total NK and separately, cytokine producing NKs (CD56bright) and cytotoxic NKs (CD56dim) were examined in 6 healthy and 11 vitiligo patients and results represented as % of total PBMC (e). The percentage of ILC1, ILC2 and ILC3 in the blood of healthy (n = 8) and vitiligo (n = 10) patients is shown in f. Results are shown as individual dot plots with a line at median (a–d) or as means ± SEM (e, f)

Article Snippet: In situ ILC1 population was detected using anti-human CD161 (green) (Novus Biological, US) and anti-Tbet (BioLegend, London, UK) (red) with the use of True-Nuclear® Transcription Factor Buffer Set (Biolegend) for nuclear staining.

Techniques: Immunohistochemistry