Dectin‐1, Toll‐like receptor (TLR)‐2 and TLR‐4 are involved differentially in high T helper type 17 (Th17) response and latency‐associated protein (LAP)+ cells expansion in multi‐drug‐resistant tuberculosis (MDR‐TB) patients. (a,b). PBMC from 10 MDR‐TB patients and six PPD+ healthy donors (HD) controls were stimulated for 48 h alone (control, C) or with Mtb strains, in the absence (–) or presence of antibodies against TLR‐2, TLR‐4 and dectin‐1 (a‐TLR‐2, a‐TLR‐4 and a‐dectin‐1). Then, the IL‐17 and interferon (IFN)‐γ expression was determined within the CD4+ subset by FACS and the number (n) of CD4+IL‐17+IFN‐γ– and of CD4+IL‐17+IFN‐γ+ cells in 1×106 cultured PBMC was calculated. Box‐plots show median and 25th–75th percentiles with maximum and minimum values; statistical differences: *P < 0·05 for treated versus non‐treated PBMC (Friedman test followed by Dunn's test). (c). PBMC from six MDR‐TB patients were stimulated for 48 h alone or with Mtb strains, in the absence (–) or presence of anti‐TLR‐2 or anti‐TLR‐4 antibodies. Then LAP expression was determined in CD4+ and CD14+ cells by FACS. Results are expressed as number (n) of CD4+LAP+ and CD14+LAP+ cells in 1 × 106 PBMC (median and 25th–75th percentiles with maximum and minimum values). Statistical differences: *P < 0·05 for antibody‐treated versus non‐treated PBMC (Friedman test followed by Dunn's test).