Rabbit Anti-Human CPB2 (a.a. 131-230) Polyclonal antibody

We have previously identified that Leishmania mexicana cysteine proteases (CPs) are virulence factors. We have now produced a recombinant L. mexicana CP, CPB2.8, which has similar enzymatic activity to native enzyme. Inoculation of CPB2.8 (less than or equal to5 mug) into the footpads of BALB/c mice not only up-regulated mRNA transcripts for IL-4 and IL-4 production in the draining popliteal lymph nodes, but also polarized splenocyte anti-CD3 stimulated responses toward a Th2 bias as measured by increased IL-5 production compared with controls. In agreement with promoting a Th2 response, CPB2.8 also induced strong specific IgE responses in treated mice as well as increasing whole IgE levels. Inhibition of the enzyme activity of CPB2.8 by treatment with E-64 ablated the enzyme's ability to induce IgE. Significantly, infection of mice with CPB-deficient parasites failed to stimulate production of IgE, unlike infection with wild-type parasites. Furthermore, enzymatically active (<0.1 U/ml) but not E-64-inactivated CPB2.8 was able to proteolytically cleave CD23 and CD25, although not B220 or CD4 from murine lymphocytes. These properties are similar to those demonstrated by the house dust mite allergen Der p I and provide an explanation for the immunomodulatory activity of the CPB2.8 virulence factor. Vaccination with CPB2.8 enhanced L mexicana lesion growth compared with control animals. Nevertheless, vaccination with IL-12 and CPB2.8 resulted in a degree of protection associated with inhibition of lesion growth and a Th1 response. Thus, CPB2.8 is a potent Th2-inducing molecule capable of significant vaccine potential if administered with a suitable adjuvant. The Journal of Immunology, 2003.

An 11-yr-old female hamadryas baboon (Papio hamadryas) that died with a history of diarrhea and anorexia was submitted for necropsy. Major pathologic changes were restricted to the gastrointestinal tract. The small intestinal contents were watery and sanguinous, With a deepening of the red color in the large intestines. The intestinal mucosa was hyperemic. Microscopically, lesions consisted of surface epithelial cell necrosis in association with numerous rod-shaped bacteria and high numbers of Trichuris cynocephalus nematodes. Culturing of the small intestine yielded Clostridium perfringens. No other pathogenic bacteria were cultured using routine bacteriologic techniques. Polymerase chain reaction (PCR) analysis classified the Clostridium perfringens as type A cpb2-positive. Immunohistochemical examination with anti-beta 2-toxin antibodies revealed beta 2-toxin in close approximation with the intestinal lesions.