الفهرس 
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Abstract
Schistosomiasis is an endemic disease refractory to itrol. Although the close relation betueen Schistosoma isoni infection and development of hepatosplenic lesion > been epidemiollogically documented in man, the biologi-. mechanisms involved in human schistosomiasis are not ly understood.
It has become increasingly obvious that chronic ection with parasitic schistosomes is associated with found modulation of the normal immunologic responses of ected hosts. The present study, uas designed to examine
modulatory immunologic functions of patients with nansoni infection -at different clinicopathological stages
its correlation with HLA typing.
In the present study the investigation uas done on ty patients with chronic Schistosoma mansoni infection, een of them manifested hepatosplenomegaly without lications (First group) and fifteen of them in the late e with complications (Second group), in addition to ten thy control individuals. The humoral immunity (specific anti SEA) uas studied by ELISA technique. The cellular nity was investigated for T cell count and function in anse to PHA and Com A mitogens and SEA antigen. Also
effect of the patient’s sera on the proliferative
response of lymphocyte was investigated. In addition the immunogenetic analysis of the specific HLA antigens were studied in patients and control groups.
Schistosomal patients represented significant increase
in specific antibodies than the normal group. As regard
the cellular immunity, the S. patients represent signifi¬
cant depression of T cell count and LPR to PHA than those
of the normal group. whereas, LPR to Con A was slightly
but not significantly higher than the normal subject.
In contrast, LPR to SEA was significantly higher in •
schistosomal group than in normal group. The percentage of
suppression of LPR as a result of the presence of P.S was.
significantly higher in response to PHA, ConA mitogens and
SEA antigen. In addition, there is positive significant
correlation between the specific antibody and percentage of
suppression of LPR to SEA. As regards to tissue typings,
S. patients showed R.R to HLA-A*, -A^, -Be + Bu7i;’”Bu3B
antigens.
On analysis these results between the two schistosomal groups, we found in the first group studied that, the specific antibody was significantly higher than the normal and second groups. The difference of T cell count in this group between the normal and second group were not signifi¬cant. LPR to PHA was significantly lower than normal and not significantly higher than the:second group. In contrast,
LPR to Con A was significantly higher than those of the
normal and second groups. Uhereas LPR to SEA uas significantly
higher than the normal group and not significantly higher
than the second group. As a result the mean percentage of
suppression of LPR to PHA uas significantly higher than
normal groups and not significantly lower than the second
group. Uhereas the mean percentage of suppression of LPR to
Con A and SEA uere significantly higher than those of
normal and second groups. As regards tissue typings, this group
showed decrease in R.R of HLA-A.., -A,, and -Br + Bu-*e. anc’
increase in R.R of HLA-Bw_fl. This HLA-Bu^fl may be in
linkage of Is gene.
In the second schistosomal group, there was significant increase in specific antibody than normal group. T cell count uas significantly louer than normal group. LPR to PHA uas significantly louer than normal groups, while LPR to Con A uas not significantly lower than normal group. In contrast LPR to SEA uas significantly higher than normal group. As a result the mean percentages of suppression of LPR to PHA, Con A and SEA were significantly higher than normal means. In tissue typings, the R.R of HLA-A.. , -A..,, and -B,- + Bu7C was increased while the R.R of HLA-Bu.,,-, decreased. Also there is linkage between these high frequent antigens in this group and bleeding in patients. Consequently there could be linkage betueen HLA-A., ”A,.., -B^+Bu^t- with