The anti-TNF biologics block the excess of a protein causing inflammation. Monoclonal antibodies, like infliximab, are engineered to bind TNF directly. Receptor-fusion proteins, like etanercept, are a decoy receptor that soaks it up.
I explain this to my patients with a weaver's analogy: one is like adding a precise new patch to a shawl, the other is like re-weaving the edge with a different thread entirely. Both mend the tear, but their *taanka*—their very structure—is different. And in my clinic, that difference decides which pattern will hold.
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