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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Biomaterials. 2021 Aug 20;277:121079. doi: 10.1016/j.biomaterials.2021.121079

Figure 4: paKG(PFK15+bc2) MPs alter DC function in vitro and in vivo in a CIA mouse model.

Figure 4:

(a) Schematic of paKG(PFK15+bc2) MPs reprogramming DC surface proteins for the modulation of adaptive immune responses. (b-e) Histogram plots of CD11c+CD86+ frequencies demonstrate that paKG-based MPs in the presence LPS have lower CD86 expression than LPS alone, (b) paKG MPs with and without LPS, (c) paKG(bc2) MPs with and without LPS, (d) paKG(PFK15) MPs with and without LPS, (e) paKG(PFK15+bc2) MPs with and without LPS. (f) In the presence of LPS, paKG-based MPs significantly decreased the frequency of CD11c+CD86+ cells in vitro as compared to LPS (n = 5–11, avg ± SEM, *- p<0.05). (g) paKG(PFK15+bc2) MPs significantly increased the percentage of CD86LoMHCII+ of CD11c+ cells in vitro as compared to no treatment and all other paKG-based MPs (n = 6–12, avg ± SEM, *- p<0.05). (h) All paKG-based MPs, in the presence of LPS, have a significantly lower frequency of CD86HiMHCII+ of CD11c+ cells in vitro as compared to LPS (n = 5–11, avg ± SEM, *- p<0.05). (i) paKG MPs encapsulating PFK15, reduce CD11c+CD86+ frequency within the MP injection sites of CIA mice (n = 4–8, avg ± SEM, *- p<0.05). (j) In vivo CD11c+ frequencies within the inguinal lymph nodes of CIA mice (n = 5–7, avg ± SEM, *- p<0.05).