A revival of the B cell paradigm for rheumatoid arthritis pathogenesis?
Dominant paradigms for the understanding of rheumatoid arthritis (RA) pathogenesis have changed over the years. A predominant role of B lymphocytes, and perhaps of the rheumatoid factor they produced, was initially invoked. In more recent years, recognition of antigens in the joint by T cells sparking an inflammatory cascade has been a more favored interpretation. Here, we re-examine some of the arguments that underpin this proposed role of joint T cells, in light of recent results from transgenic mice in which a self-reactive T-cell receptor provokes disease, but from outside the joint and indirectly via B lymphocytes and immunoglobulins.
Complete Metadata
| @type | dcat:Dataset |
|---|---|
| accessLevel | public |
| bureauCode |
[
"009:25"
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{
"fn": "NIH",
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"hasEmail": "mailto:info@nih.gov"
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|
| description | Dominant paradigms for the understanding of rheumatoid arthritis (RA) pathogenesis have changed over the years. A predominant role of B lymphocytes, and perhaps of the rheumatoid factor they produced, was initially invoked. In more recent years, recognition of antigens in the joint by T cells sparking an inflammatory cascade has been a more favored interpretation. Here, we re-examine some of the arguments that underpin this proposed role of joint T cells, in light of recent results from transgenic mice in which a self-reactive T-cell receptor provokes disease, but from outside the joint and indirectly via B lymphocytes and immunoglobulins. |
| distribution |
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|
| identifier | https://healthdata.gov/api/views/n3th-rnt4 |
| issued | 2025-07-14 |
| keyword |
[
"b-lymphocytes",
"immunoglobulins",
"nih",
"rheumatoid-arthritis",
"t-lymphocytes"
]
|
| landingPage | https://healthdata.gov/d/n3th-rnt4 |
| modified | 2025-09-06 |
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| publisher |
{
"name": "National Institutes of Health",
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|
| theme |
[
"NIH"
]
|
| title | A revival of the B cell paradigm for rheumatoid arthritis pathogenesis? |
