scholarly journals The response of T cells to interleukin-6 is differentially regulated by the microenvironment of the rheumatoid synovial fluid and tissue

2011 ◽  
Vol 63 (11) ◽  
pp. 3284-3293 ◽  
Author(s):  
Ester Hidalgo ◽  
Sarah J. Essex ◽  
Lorraine Yeo ◽  
S. John Curnow ◽  
Andrew Filer ◽  
...  
2007 ◽  
Vol 122 (1) ◽  
pp. 28-40 ◽  
Author(s):  
María José Martínez-Lorenzo ◽  
Alberto Anel ◽  
Berta Saez-Gutierrez ◽  
María Royo-Cañas ◽  
Alberto Bosque ◽  
...  

1994 ◽  
Vol 37 (11) ◽  
pp. 1627-1636 ◽  
Author(s):  
Sheldon M. Cooper ◽  
Karen D. Roessner ◽  
Mikako Naito-Hoopes ◽  
Diantha B. Howard ◽  
Lakshmi K. Gaur ◽  
...  

2021 ◽  
pp. 155633162199200
Author(s):  
Ravi Gupta ◽  
Anil Kapoor ◽  
Sourabh Khatri ◽  
Dinesh Sandal ◽  
Gladson David Masih

Background: Osteoarthritis (OA) in the anterior cruciate ligament (ACL)–deficient knee is seen in approximately 50% of affected patients. Possible causes include biochemical or biomechanical changes. Purpose: We sought to study the correlation between inflammatory cytokines and chondral damage in ACL-deficient knees. Methods: Seventy-six male patients who underwent ACL reconstruction were enrolled in a cross-sectional study. Synovial fluid was aspirated before surgery and analyzed for levels of the inflammatory cytokines tumor necrosis factor-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). At the time of ACL reconstruction, the severity of chondral damage was documented as described by the Outerbridge classification. Results: Patients with grade 2 or higher chondral damage were observed to have elevated IL-6 levels when compared to patients who had no chondral damage. Interleukin-6 levels had no correlation with the duration of injury. Conclusion: Elevated levels of IL-6 in synovial fluid were associated with chondral damage in ACL-deficient knees. Further study is warranted to determine whether inflammatory cytokines contribute to the development of OA of the knee after ACL injury.


2021 ◽  
Vol 9 (7) ◽  
pp. e002716
Author(s):  
Sang T. Kim ◽  
Jean Tayar ◽  
Siqing Fu ◽  
Danxia Ke ◽  
Elliot Norry ◽  
...  

With durable cancer responses, genetically modified cell therapies are being implemented in various cancers. However, these immune effector cell therapies can cause toxicities, including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Pseudogout arthritis is an inflammatory arthritis induced by deposition of calcium pyrophosphate dihydrate crystals. Here, we report a case of pseudogout arthritis in a patient treated with MAGE-A4 directed T cell receptor T cells, for fallopian tube cancer. The patient developed CRS and ICANS 7 days after infusion of the T cells. Concurrently, the patient newly developed sudden onset of left knee arthritis. Synovial fluid analyses revealed the presence of calcium pyrophosphate dihydrate crystal. Notably, the pseudogout arthritis was resolved with tocilizumab, which was administered for the treatment of CRS and ICANS. Immunoprofiling of the synovial fluid showed that the proportion of inflammatory interleukin 17 (IL-17)-producing CD4+ T (Th17) cells and amount of IL-6 were notably increased, suggesting a potential role of Th17 cells in pseudogout arthritis after T-cell therapy. To the best of our knowledge, this is the first reported case of pseudogout arthritis after cell therapy. Clinicians, especially hematologists, oncologists and rheumatologists, should be aware that pseudogout arthritis can be associated with CRS/ICANS.


1989 ◽  
Vol 19 (11) ◽  
pp. 2107-2114 ◽  
Author(s):  
Pierre G. Coulie ◽  
Monique Stevens ◽  
Jacques Van Snick

1991 ◽  
Vol 21 (9) ◽  
pp. 2139-2143 ◽  
Author(s):  
Elisabeth Hermann ◽  
Ansgar W. Lohse ◽  
Ruurd Van Der Zee ◽  
Willem Van Eden ◽  
Werner J. Mayet ◽  
...  

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