Publication date: Oct 11, 2024
Incomplete Freund’s adjuvant (IFA) has long been used to trigger autoimmune diseases in animal models, such as experimental autoimmune encephalitis and collagen-induced arthritis. However, the molecular mechanisms that control CD4 T cell effector functions and lead to the development of autoimmune diseases are not well understood. A self-antigen and heat-killed Mycobacterium tuberculosis emulsified in IFA augmented the activation of CD4 T cells, leading to the differentiation of pathogenic CD4 T cells in the draining lymph nodes. In contrast, IFA emulsification did not elicit Foxp3 regulatory T cell expansion. We found that pathogenic Th1 cells expressed miR-147-3p, which targets multiple genes to affect T cell function. Finally, miR-147-3p expressed in CXCR6SLAMF6 Th1 cells was required for the onset of neurological symptoms through the control of CXCR3 expression. Our findings demonstrate that miR-147-3p expressed in pathogenic CD4 T cells regulates the migratory potential in peripheral tissues and impacts the development of autoimmune diseases.
Concepts | Keywords |
---|---|
Autoimmune | Autoimmune diseases |
Foxp3 | CD4 T cells |
Models | CXCR3 |
Mycobacterium | Incomplete Freund’s adjuvant |
Tuberculosis | miR-147-3p |
Semantics
Type | Source | Name |
---|---|---|
disease | IDO | cell |
disease | MESH | collagen-induced arthritis |
disease | MESH | autoimmune encephalitis |
disease | MESH | autoimmune diseases |