These effects are mediated through the NRP2/NF-κB/TNFα axis, which also underlies NRP2-induced sorafenib resistance. Targeting this axis with the TNF-α inhibitor adalimumab effectively reversed sorafenib resistance in ccRCC, suggesting a promising therapeutic strategy.
This combination also exhibited synergistic improvement in colitis severity in treated mice. These findings underscore the therapeutic potential of B. thetaiotaomicron in IBD, either alone or in combination with infliximab, and support further development of microbiota-based strategies for IBD prevention and treatment.
Bimekizumab treatment resulted in consistent, sustained efficacy to 52 weeks in biologic-naïve and TNFi-IR individuals with PsA and baseline plaque-type psoriasis and nail involvement. Bimekizumab was well tolerated, with a safety profile consistent with previous reports. Graphical abstract available for this article.
Ozoralizumab has the potential to improve disease activity and physical dysfunction and prevent joint destruction in patients, regardless of the presence of LJI, and is a reasonable treatment option, even for patients with LJI.
In summary, we ascertain that treatment with TNF inhibitors does not affect Th1, Th2, or Th17 responses. Etanercept and monoclonal antibodies differ in their effect on IL-17A+DN T cells.
One quarter of IBD patients requiring intensified anti-TNFa therapie were successfully deescalated to standard dosing, after a median of 16.0 (IQR: 8.0-36.0) months.
New therapeutic options to reduce the red blood cell (RBC) transfusion burden have emerged since 2020 and include luspatercept and imetelstat. Erythropoiesis-stimulating agents and lenalidomide also address anemia and are generally recommended to start at the time of transfusion dependency, although emerging data suggest that an earlier start of these interventions might offer clinical benefits...Targeted therapy directed to the presence of an IDH1 mutation is U.S. Food and Drug Administration (FDA) approved for the rare IDH1 mutated MDS (<10% of the time) and consideration to use an IDH2 inhibitor for IDH2 mutated MDS (<5% of the time) is reasonable. Interestingly, IDH mutations seem to appear with increased frequency in older patients and in patients with underlying autoimmune/rheumatological disorders.1.