A newly identified type of T cells, involved in the development of rheumatoid arthritis, could hold the key to understanding the immune response that underlies type 1 diabetes.
The researchers from Harvard Medical School, who made the discovery, reported in the journal Nature that this type of T cell could be responsible for causing most of the damage in joints affected by rheumatoid arthritis.
Previous research has shown that the inflammation and destruction of joint tissue in rheumatoid arthritis occurs when T cells interact with the immune regulators B lymphocytes, or B cells, instead of just fighting pathogens.
Until now, scientists knew that these aberrant interactions is what produces antibodies leading to tissue damage, but different kinds of T cells exist and it was unclear which ones were implicated.
To find out, the researchers looked at the profile of T cells most abundantly found in injured joint tissue of patients with rheumatoid arthritis.
High tech tools, such as cytometry and RNA sequencing, were used to analyse samples of cells from the damaged joint tissue, as well as the blood and fluid surrounding joints.
The cytometry technique helped to determine which T cells express factors enabling B cell help, while the RNA sequencing allowed the researchers to see if there is activation of certain genes associated with the migration of T cells to inflamed areas.
What they found is that helper T cells, known as CD4+, were overrepresented in the damaged tissue of participants. They accounted for around a quarter of the T cells there.
These T cells also appeared to be genetically programmed to infiltrate parts of the body that are inflamed, where they then stimulate B cells to produce even more antibodies.
The findings have left researchers with many more unanswered questions about these rogue T cells, namely how do they develop and whether or not they are involved in other autoimmune diseases, including type 1 diabetes, lupus, and multiple sclerosis.
In type 1 diabetes, it is believed that the activation of damaging T cells to beta cell pancreatic islets, and their capacity to infiltrate them, may rely partly on help from CD4+ T cells.

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