Monoclonal antibodies used for inflammatory bowel disease include infliximab and adalimumab, both of which are directed against TNFalpha (FA2020 p382, 122, 487)
Another way of thinking about this is to think about common therapeutic antibodies used as well as the function of the other things listed to eliminate them. TNFalpha is commonly blocked by biologics for therapy in autoimmune and inflammatory disease, and generally it makes sense it would be beneficial to block as it is one of the primary pro-inflammatory cytokines
Bradykinin is involved in inflammation but has no major therapeutic Abs targeting it. C5a is an anaphylotoxin, and though monoclonal antibodies targeting C5 do exist they are used to treat paroxysmal noturnal hemoglobinuria. C5a does not play a major role in the pathogenesis of IBD. Blocking class I MHC antigens does not make sense, as antigens are what elicit the immune response and are presented to T-cells and there are millions of possible antigens that could be presented that are eliciting the inflammatory response. If you block class I MHC ittself it would also be extremely detrimental as then CD8 T-cells would not be able to respond to any infection/etc. Fibrin is involved in the clotting pathway and would not be beneficial to block in IBD. PGE2 is associated with pain, but it is not targeted by any therapeutic antibodies.
submitted by โcassdawg(1779)
Monoclonal antibodies used for inflammatory bowel disease include infliximab and adalimumab, both of which are directed against TNFalpha (FA2020 p382, 122, 487)
Another way of thinking about this is to think about common therapeutic antibodies used as well as the function of the other things listed to eliminate them. TNFalpha is commonly blocked by biologics for therapy in autoimmune and inflammatory disease, and generally it makes sense it would be beneficial to block as it is one of the primary pro-inflammatory cytokines
Bradykinin is involved in inflammation but has no major therapeutic Abs targeting it. C5a is an anaphylotoxin, and though monoclonal antibodies targeting C5 do exist they are used to treat paroxysmal noturnal hemoglobinuria. C5a does not play a major role in the pathogenesis of IBD. Blocking class I MHC antigens does not make sense, as antigens are what elicit the immune response and are presented to T-cells and there are millions of possible antigens that could be presented that are eliciting the inflammatory response. If you block class I MHC ittself it would also be extremely detrimental as then CD8 T-cells would not be able to respond to any infection/etc. Fibrin is involved in the clotting pathway and would not be beneficial to block in IBD. PGE2 is associated with pain, but it is not targeted by any therapeutic antibodies.