<i>Mycobacterium tuberculosis</i> Impairs Human Memory CD4  T Cell Recognition of Macrophages Differentiated Using M-CSF But Not GM-CSF

Analysis of alpha‐1‐antitrypsin (AAT)‐regulated, glucocorticoid receptor‐dependent genes in macrophages reveals a novel host defense function of AAT

“…Repleting M-CSF during MTB infection decreased the number of foamy macrophages, increased class II MHC molecules on the alveolar macrophages, increased expression of the pattern-recognition receptor DEC-205, and increased their T cell stimulating capacity. This activating effect of M-CSF on T cells in mice (Higgins et al, 2008) is in contradistinction to that seen in primary human cells (Gail et al, 2023). However, others implicate GM-CSF as being more protective than M-CSF in mice against mycobacterial infections.…”

“…In coculture of invariant natural killer T (iNKT) cells and macrophages, production of GM-CSF by the iNKT cells enhanced control of MTB infection in the macrophages (Rothchild et al, 2014). Gail and co-workers (Gail et al, 2023) showed in primary human macrophages and T cells that MTB-infected macrophages that were differentiated with GM-CSF (more M1-like) were better able to activate T cells than MTB-infected macrophages that were differentiated with M-CSF, which were more M2-like. Such dichotomy is likely an oversimplification as there are many genes that are induced or inhibited in macrophages in a similar fashion by GM-CSF or M-CSF (Martinez & Gordon, 2014).…”