TY - JOUR
T1 - Specific T cell unresponsiveness in human filariasis
T2 - diversity in underlying mechanisms
AU - SARTONO, ERLIYANI
AU - KRUIZE, YVONNE C.M.
AU - PARTONO, FELIX
AU - Kurniawan, Agnes
AU - MAIZELS, RICK M.
AU - YAZDANBAKHSH, MARIA
PY - 1995/11
Y1 - 1995/11
N2 - In an attempt to overcome T cell unresponsiveness to filarial antigens, 65 individuals belonging to the three clinical groups of elephantiasis patients, microfilaraemics, and asymptomatic amicrofilaraemics who exhibited unresponsiveness to Brugia malayi adult worm antigen (BmA) were studied. Peripheral blood mononuclear cells were co‐cultured with antigen and one of the following reagents that have been reported to be effective in reconstituting T cell proliferation: interleukin‐2 (IL‐2), interleukin‐7 (IL‐7), anti‐interleukin‐4, anti‐interleukin‐10, anti‐CD2, anti‐CD27, anti‐CD28, indomethacin, phorbol myristate acetate (PMA), or calcium ionophore (A23I87). We were able to overcome antigen‐specific unresponsiveness in only a minority of the individuals studied. Co‐culture with IL‐2, IL‐7, indomethacin and PMA were the only conditions which resulted in enhanced proliferation to BmA in these individuals. In general, unresponsiveness in elephantiasis patients was easier to reverse than in other clinical groups: in 50% of elephantiasis patients, in 12.5% of microfilaraemics and in 20% of asymptomatic amicrofilaraemics. The results indicate that more than one distinct immunological mechanism may account for the antigen‐specific unresponsiveness in individuals exposed to and infected with brugian filariasis.
AB - In an attempt to overcome T cell unresponsiveness to filarial antigens, 65 individuals belonging to the three clinical groups of elephantiasis patients, microfilaraemics, and asymptomatic amicrofilaraemics who exhibited unresponsiveness to Brugia malayi adult worm antigen (BmA) were studied. Peripheral blood mononuclear cells were co‐cultured with antigen and one of the following reagents that have been reported to be effective in reconstituting T cell proliferation: interleukin‐2 (IL‐2), interleukin‐7 (IL‐7), anti‐interleukin‐4, anti‐interleukin‐10, anti‐CD2, anti‐CD27, anti‐CD28, indomethacin, phorbol myristate acetate (PMA), or calcium ionophore (A23I87). We were able to overcome antigen‐specific unresponsiveness in only a minority of the individuals studied. Co‐culture with IL‐2, IL‐7, indomethacin and PMA were the only conditions which resulted in enhanced proliferation to BmA in these individuals. In general, unresponsiveness in elephantiasis patients was easier to reverse than in other clinical groups: in 50% of elephantiasis patients, in 12.5% of microfilaraemics and in 20% of asymptomatic amicrofilaraemics. The results indicate that more than one distinct immunological mechanism may account for the antigen‐specific unresponsiveness in individuals exposed to and infected with brugian filariasis.
KW - T cells
KW - co‐stimulation
KW - filariasis
KW - unresponsiveness
UR - http://www.scopus.com/inward/record.url?scp=0029561440&partnerID=8YFLogxK
U2 - 10.1111/j.1365-3024.1995.tb01002.x
DO - 10.1111/j.1365-3024.1995.tb01002.x
M3 - Article
C2 - 8817605
AN - SCOPUS:0029561440
SN - 0141-9838
VL - 17
SP - 587
EP - 594
JO - Parasite Immunology
JF - Parasite Immunology
IS - 11
ER -