TY  - JOUR
ID  - open3242
UR  - http://crdd.osdd.net/open/3242/
IS  - 2
A1  - Lamba, Taruna
A1  - Zafar, Mohammad Adeel
A1  - Shaaz, Mohammad
A1  - Singh, Sanpreet
A1  - Singh, Sudhakar
A1  - Khan, Mohd Affan
A1  - Prajapati, Shivank
A1  - Malik, Junaid A
A1  - Nanda, Sidhanta
A1  - Siddiqui, Kaneez F
A1  - Arora, Ashish
A1  - Sehrawat, Sharvan
A1  - Agrewala, Javed N
Y1  - 2025///
N2  - Mycobacterium tuberculosis (Mtb) effectively suppresses host immunity to ensure its survival. We have earlier shown that the Acr1 protein of Mtb can inhibit the differentiation of dendritic cells (DCs). Consequently, in the current study, we examined the role of Acr1 in mitigating autoimmunity. Initially, we observed that Acr1 skews the differentiation of DCs into functionally competent myeloid-derived suppressor cells (MDSCAcr1) that chiefly secrete immunosuppressive molecules, expand regulatory T cells (TregAcr1) and attenuate inflammatory responses. Further, MDSCAcr1 suppress Th17 cells. Acr1 expanded MDSCs with a concurrent increase in myelin oligodendrocyte glycoprotein (MOG)-specific Tregs and a decline in Th17 cells in a murine experimental autoimmune encephalomyelitis (EAE) model and prevented the onset of the disease. These results were further validated in the prophylactic model of EAE. Mechanistically, Acr1 activates Tregs and MDSCs via the TLR-4 pathway, implicating innate immune recognition in Mtb-induced suppression. The results indicate a potential role of Acr1 against autoimmune diseases.
PB  - Wiley
JF  - Immunology
VL  - 177
KW  - Mycobacterium tuberculosis ; Acr1; TLR4; Tregs; autoimmunity; experimental autoimmune encephalomyelitis; myeloid-derived suppressor cells
TI  - Mycobacterium tuberculosis Acr1 protein mitigates experimental autoimmune encephalomyelitis symptoms by generating myeloid-derived suppressor cells and regulatory T cells
SP  - 370
EP  - 383
ER  -