Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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The regulatory factors involved in rheumatoid arthritis (RA) complicated with interstitial lung disease (ILD) (RA-ILD) remain unknown. Due to the cross-sectional nature of our study, our aim was to explore the role of the signalling lymphocytic activation molecule family (SLAMF) in RA-ILD by analysing synovial and lung samples from the Gene Expression Omnibus, animal models, and clinical samples.We collected peripheral blood mononuclear cells from patients for flow cytometry analysis of B cells, SLAMF1 protein, and SLAMF7 protein. The dataset analysis indicated a marked upregulation of SLAMF1 and SLAMF7 expression in RA synovial tissues and RA-ILD lung tissues. The same expression trend was further validated in a collagen-induced arthritis-ILD model. This suggests that B cells expressing SLAMF1 and SLAMF7 may contribute significantly to the development of lung fibrosis. Flow cytometry analysis demonstrated that SLAMF7 expression in B cells was substantially higher in RA-ILD patients than in those with RA alone. Similarly, SLAMF7 proteins were highly expressed in the plasma of patients with RA-ILD. These results suggest that SLAMF7 could be pivotal in the development and progression of RA-ILD.
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http://dx.doi.org/10.1016/j.intimp.2025.114392 | DOI Listing |