Figure 5. The Absence of IL-17A Signaling Enables Ly6C^lo Monocyte-to-Macrophage Differentiation In vivo.

(A) Schematics of intracardiac injection of CD45.2⁺Ly6C^hi or CD45.2⁺Ly6C^lo monocytes into CD45.1 day 21 EAM IL-17Ra^−/− recipient mice.

(B and C) Gating of concatenated Ly6C^hi (B) and Ly6C^lo (C) donor cells from the total viable CD115⁺CD11b⁺ population.

(D) Percentages of injected Ly6C^hi or Ly6C^lo MDMs.

(E and F) Frequencies of Ly6C^hi MDMs (E) and Ly6C^lo MDMs (F) out of the viable CD45.2⁺CD115⁺CD11b⁺ population.

(G and H) F4/80 and CD64 expression intensities of Ly6C^hi (G) and Ly6C^lo (H) MDMs using bh-SNE-dimensional reduction algorithm.

(I) Schematics of retro-orbital injection of CD45.1⁺Ly6C^lo monocytes into CD45.2 day 21 EAM WT or IL-17Ra^−/− recipient mice.

(J) Gating of concatenated Ly6C^lo donor cells from the total viable CD115⁺CD11b⁺ population in WT and in IL-17Ra^−/− recipient ice.

(K) CD45.1⁺ monocytes were gated based on no injection control CD45.2⁺ mice.

(L) Percentages of CD45.1+ Ly6C^lo MDMs in the heart.

(M) Frequencies of Ly6C^lo MDMs out of the viable CD45.1⁺CD115⁺CD11b⁺ population in WT and in IL-17Ra^−/− recipient mice. Data are representative of two independent experiments with biological triplicates.

(D and L) n = 3. Groups were compared using Student’s t test. *p < 0.05, **p < 0.01. All data were presented as mean ± SD.

See also Figure S5.