Lamba, Taruna and Zafar, Mohammad Adeel and Shaaz, Mohammad and Singh, Sanpreet and Singh, Sudhakar and Khan, Mohd Affan and Prajapati, Shivank and Malik, Junaid A and Nanda, Sidhanta and Siddiqui, Kaneez F and Arora, Ashish and Sehrawat, Sharvan and Agrewala, Javed N (2025) Mycobacterium tuberculosis Acr1 protein mitigates experimental autoimmune encephalomyelitis symptoms by generating myeloid-derived suppressor cells and regulatory T cells. Immunology, 177 (2). pp. 370-383.
Full text not available from this repository.Abstract
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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | Mycobacterium tuberculosis ; Acr1; TLR4; Tregs; autoimmunity; experimental autoimmune encephalomyelitis; myeloid-derived suppressor cells |
| Subjects: | Q Science > QR Microbiology |
| Depositing User: | Dr. K.P.S.Sengar |
| Date Deposited: | 01 Feb 2026 14:11 |
| Last Modified: | 02 Feb 2026 07:42 |
| URI: | http://crdd.osdd.net/open/id/eprint/3242 |
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