DIFFERENTIAL RECOGNITION OF MICROFILARIAL CHITINASE, A TRANSMISSION-BLOCKING VACCINE CANDIDATE ANTIGEN, BY SERA FROM PATIENTS WITH BRUGIAN AND BANCROFTIAN FILARIASIS
S. Dissanayake et al., DIFFERENTIAL RECOGNITION OF MICROFILARIAL CHITINASE, A TRANSMISSION-BLOCKING VACCINE CANDIDATE ANTIGEN, BY SERA FROM PATIENTS WITH BRUGIAN AND BANCROFTIAN FILARIASIS, The American journal of tropical medicine and hygiene, 53(3), 1995, pp. 289-294
Citations number
28
Categorie Soggetti
Public, Environmental & Occupation Heath","Tropical Medicine
We examined the reactivity of human sera with recombinant microfilaria
l chitinase and with the anti genic determinant on the native parasite
molecule identified by monoclonal antibody (MAb) MF1. In Brugian fila
riasis, the MF1 epitope is preferentially recognized by residents of e
ndemic areas who remain amicrofilaremic and asymptomatic despite lifel
ong exposure to filarial worms. Reactivity with filarial chitinase and
its MF1 epitope inversely correlates with microfilaremia levels in Ba
ncroftian filariasis and is associated with a prolonged amicrofilaremi
c state following a single course of treatment with diethylcarbamazine
. Chitinase does not appear to be a target of human antibodies that pr
omote the adherence of cells to microfilariae, even though MAb MF1 its
elf promotes antibody-dependent, cell-mediated cytotoxic (ADCC) reacti
ons that kill microfilariae in vitro. Such ADCC reactions are most oft
en mediated by sera from amicrofilaremic patients with chronic elephan
tiasis that contain low or undetectable levels of IgG antibodies to ch
itinase. In contrast, antibodies to the MF1 epitope on this microfilar
ial stage-specific antigen are mostly present in amicrofilaremic donor
s without clinical lymphatic disease. These observations indicate that
antibodies to the MF1 epitope of microfilarial chitinase reflect some
degree of immune resistance to microfilaremia in a subgroup of patien
ts with asymptomatic lymphatic filariasis. The amicrofilaremic state o
f individuals with chronic lymphatic disease appears to be mediated by
reactivity to a different parasite antigen(s).