الفهرس 
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Abstract
In tris work we demonstrated the inhibition oflymphocyte proliferation (measured by DNA synthesis) bythe immunosuppressive substance (ISS) present in the Smansoni incubation product and released by the adult wormsThe ISS was not species-specific (in rat, mouse and humanresistant to heating, dialyzable and of low molecularweight (500 - 10CO) Our results could be s wnmarize d in the following 1. The prepared ISS has an inhicitory activity on
tbe lymphocyte proliferation of normal Fischer rats after
being injected with it (group B) •
2. Studying the lymphocytic response of infected
Fischer rats with S. mansoni (group D) showed clearly
that there are two stages of lymphocytic activity;first;
enhanced lymphocyte reactivity at day 10 - 14 after infection,
and second; characterized by a lowered lymphocyte
reactivity during the 5th week (day 35).
J. Injecting Fischer rats with the ISS after infection
w.i t h S. mansoni (group C) decreased the lymphocyte
proliferation at the erhanced stage (day 10 - 14) and
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.inc r-e as ed the inhibition at the unresponsive stage (day
35), if compared with control infected group D, i.e. the
ISS increased the overall suppression or inhibition.
4. Purification -- rat spleen cells by platting on
plastic surface of Petri dish for 2 hr. then incubated
in nylon wool column at the unresponsive stage did not
restore the lymphocyte response to can. A or to S.rnansoni
antigen.
The inhibition in lymphocyte proliferation that
occurred during the 5th week either due to the normal S.
mans ani infection (group D) or artificially due to the
injected ISS (group B & C), does not involve any specific
or non-specific suppressor cells. Either inhibitory
stimuli were found to act diretly on the responder lymphocytes
even after removal of macrophageg and T-suppressor
cells.
Our work succeeded in throwing some light on the
host-parasite relationship in Bilharzial infection. It
also evaluated the parameters of the initial stimulation
associated with infection of S.mansoni followed by a
remarkable depression in lymphocytic response; this might
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be due to the ISS re13as3d by the adult worms at that
stage of infection and which has proved to have a direct
effect on the responder lymphocytes and not through the
induction of suppressor cells or by modification of macrophages
inhibitory facto~s.
Summing up our experimental results would allow us
to consider that S. mansoni could regulate the host immune
response by the release of antagonistic factors having a
predominantly irr~unosuppressive effect either directly on
responsive lymphocytes or indirectly by modulation of
suppressor T cell function. These observations might
explain some inconsistant results in passive serum transfer,
and also the fail~~e of protective immunity induction
after immunization with different crude parasite extracts.