Antibody phage display is a key tool for the development of monoclonal antibodies against various targets. However, the development of anti-peptide antibodies is a challenging process due to the small size of peptides for binding. This makes anchoring of peptides a preferred approach for panning experiments. A common approach is by using streptavidin as the anchor protein to present biotinylated peptides for panning. Here, we propose the use of recombinant expression of the target peptide and an immunogenic protein as a fusion for panning. The peptide inhibitor of trans-endothelial migration (PEPITEM) peptide sequence was fused to the Mycobacterium tuberculosis (Mtb) α-crystalline (AC) as an anchor protein. The panning process was carried out by subtractive selection of the antibody library against the AC protein first, followed by binding to the library to PEPITEM fused AC (PEPI-AC). A unique monoclonal scFv antibodies with good specificity were identified. In conclusion, the use of an alternative anchor protein to present the peptide sequence coupled with subtractive panning allows for the identification of unique monoclonal antibodies against a peptide target.
Polyarteritis nodosa (PAN) is a systemic necrotising vasculitis preferentially targeting medium-sized arteries and not related with glomerulonephritis or small vessel involvement. Clinical manifestations of PAN are multisystem. The gastrointestinal, renal, cardiac, musculoskeletal, skin and central nervous systems may be involved. The aetiology remains unknown, and the ensuing vasculitis may lead to aneurysm formation and thrombosis in any organs of the body with resultant ischaemia. PAN of the intestines is a relatively common manifestation of this disease but rarely causes bowel ischaemia resulting in necrosis. Here we report a case of a young Chinese patient who presented with an acute abdomen requiring surgery and made good recovery post operatively. He remains free of symptoms while on steroid therapy.
A 37-year-old Chinese male presented with an acute abdomen. Surgical exploration revealed duodenal perforation, extensive small bowel infarction and peritonitis. Histopathology of the resected bowel showed characteristic features of classic polyarteritis nodosa. The latter also involved mesenteric arteries in the form of tiny aneurysms. Steroids could not be started due to: (i) overwhelming microbial infections and (ii) fear of more perforations in other areas of the bowel. Such a presentation of polyarteritis nodosa is uncommon. Its recognition prior to surgery, management and prognosis is discussed.