Ectopic lymphoid follicles
(place where antibody producing B cells are generated) are hallmarks of chronic autoimmune inflammatory diseases such as multiple sclerosis
(MS), rheumatoid arthritis, Sjögren's syndrome, and myasthenia gravis. However, the effector cells and mechanisms that induce their development are unknown.
Here we showed that in experimental autoimmune encephalomyelitis (EAE), the animal model of MS, Th17
( a subset of white blood cell that produces interleukin 17 that is thought to drive autoimmunity) cells specifically induced ectopic (In this context not in the lymphoid organs) lymphoid follicles in the central nervous system (CNS). Development of ectopic lymphoid follicles was partly dependent on the cytokine interleukin 17 (IL-17) and on the cell surface molecule Podoplanin
, which was expressed on Th17 cells, but not on other effector T cell subsets. Podoplanin was also crucial for the development of secondary lymphoid structures: Podoplanin-deficient mice lacked peripheral lymph nodes and had a defect in forming normal lymphoid follicles and germinal centers in spleen and lymph node remnants. Thus, Th17 cells are uniquely endowed to induce tissue inflammation, characterized by ectopic lymphoid follicles within the target organ.
The B cell that make the antibodies are found in structures called "ectopic lymphoid follicle-like structures" in the coverings of the brain and spinal cord; the covering are called the meninges.