Hypergammaglobulinaemia in Leishmania donovani infected hamsters: possible association with a polyclonal activator of B cells and with suppression of T cell function
Bunn-Moreno, M.M.; Madeira, E.D.; Miller, K.; Menezes, J.A.; Campos-Neto, A.
Clinical and Experimental Immunology 59(2): 427-434
1985
ISSN/ISBN: 0009-9104 PMID: 3872189 Document Number: 261320
Studies were carried out on the mechanisms by which B lymphocytes are polyclonally activated to secrete antibodies during visceral leishmaniasis. Crude extracts of L. donovani, the etiological agent of this disease, of L. mexicana amazonensis, the etiolgical agent of cutaneous leishmaniasis, and of Herpetomonas muscarum, a related non-pathological organism, all contain components which cause strong in vitro polyclonal activation of hamster spleen cells leading to the production of antibodies. However, in vivo, only hamsters infected with L donovani develop hypergammaglobulinemia due to B cell polyclonal activation. Hamsters injected with the crude extracts of leishmania or infected with L. mexicana amazonensis do not manifest these alterations in their B cell response. Spleen cells of hamster infected with L. donovani became unresponsive to stimulation with the T cell mitogen phytohemagglutinin (PHA) by day 10 of infection, whereas their response to concanavalin A was preserved. The decreased lymphocyte response to PBA coincided with the augmentation of the plaque-forming cell/spleen cell ratio. Spleen cells from hamsters infected with L. mexicana amazonensis responded normally to both mitogens throughout the course of infection. The hypergammaglobulinemia present in visceral leishmaniasis may be the consequence of an imbalance of regulatory T cells, possibly associated with a direct stimulation of hamster of B cells by L. donovani components.