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OX40-expressing follicular helper T cells can control rheumatoid arthritis

New study shows that a subset of follicular helper T cells contributes to the hyposialylation of autoantibodies in rheumatoid arthritis.

While investigating the role of follicular helper T cells in the onset of rheumatoid arthritis, a research team from the University of Tsukuba, Japan, have found that OX40-expressing follicular helper T cells contributed to inflammation by regulating a chemical modification of autoantibodies known as sialylation.

“Sialylation of autoantibodies has been shown to contribute to the onset of experimental arthritis in mice, through a subset of T helper cells,” said Isao Matsumoto, corresponding author on the study. “Because OX40-expressing (IL-17-producing) follicular helper T cells are present at increased proportions in patients with rheumatoid arthritis, we suspected that these cells may play a role in sialylation that promotes the development of rheumatoid arthritis.”

The study showed increased numbers of OX40-expressing (IL-17-producing) follicular helper T cells were found during the onset of experimental arthritis, accompanied by autoantibodies with an increased ability to activate immune cells in vitro. Analysis of the autoantibodies revealed that changes in sialylation caused this increased inflammatory potential, suggesting that the process of sialylation may provide a useful drug target for treatment of rheumatoid arthritis.

…blocking this interaction could reduce autoimmune inflammation while preserving immune interactions necessary for controlling potential infections

In addition to blocking the interaction between cells that could lead to increased inflammation via autoantibodies, the researchers found that this blocking strategy could reduce the numbers of follicular helper T cells in mice, which may contribute to extended resolution of arthritis symptoms.”Our analyses revealed that the interaction between OX40 on the surface of follicular helper T cells and OX40L on antibody-producing B cells led to reduction of sialylation on autoantibodies in mice,” added lead author Izumi Kurata. “We found that blocking this interaction could reduce autoimmune inflammation while preserving immune interactions necessary for controlling potential infections.”

The study was published in Annals of the Rheumatic Diseases.

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