In evaluating a 34-year-old woman with tuberculosis, which therapy's primary action involves inhibiting TNF-alpha?

Infliximab is a monoclonal antibody that specifically targets and inhibits tumor necrosis factor-alpha (TNF-alpha), a cytokine involved in systemic inflammation. Infliximab binds to TNF-alpha, preventing it from interacting with its receptors on the surface of cells. This action helps reduce inflammation in various autoimmune diseases, such as rheumatoid arthritis and Crohn's disease, making it effective in managing conditions where TNF-alpha plays a significant role in the inflammatory process.

In the context of a patient with tuberculosis, inhibiting TNF-alpha can be a double-edged sword. On one hand, it may be necessary to control inflammation; on the other hand, TNF-alpha is crucial for an effective immune response against infections like tuberculosis. While the use of infliximab could be considered in certain autoimmune conditions, caution is warranted in patients with active infections due to the risk of further complications.

In contrast, therapies such as azathioprine and rituximab do not primarily act through TNF-alpha inhibition, focusing instead on other mechanisms of immune modulation. Corticosteroids have broad anti-inflammatory effects but do not specifically inhibit TNF-alpha; their action is more generalized across various inflammatory mediators. Therefore, infliximab