Apoptosis is programmed cell death without induction of an inflammatory response. It
is mediated by Fas–a cell surface protein which is expressed on activated
lymphocytes. Interaction with its counterpart- the FasL induces the apoptosis of Fas
bearing cells. The mechanismunderlying successful immunotherapy has not been
identified. The aim of the present work was to investigate whether immunotherapy
affect Fas expression on T lymphocytes in asthmatic patients and to investigate its
potential ability to shift the Th1/Th2 balance ofimmune response to allergic reaction
in asthmatic airway. The study was conducted on 30 asthmatic subjects and 10
healthy control subjects. The asthmatic patients were treated with immunotherapy for
more than one year. Blood samples were collected at basal time (before treatment)
and one year after therapy (the end of the building up phase). The percentage of
positive T cells expressing Fas on its surface was determined using flow cytometryic
analysis technique. The expression of Fas on asthmatic patients was significantly
higher than in control subjects which decreases after immunotherapy but showing no
evidence of apoptosis, levels of IgE, IL-4 were decreased significantly after treatment,
also, level of IFN-γwas increased significantly.Conclusion:although high
percentage of the Fas expressed in studied asthmatic group but with no clear
evidence of apoptosis, may be a non concomitant increase in FasL which interfere
with the apoptotic process in such asthmatics and might be a contributing factor in
asthma pathogenesis. Thus, the lack of parallel increase of FasL to the increased Fas
could explain the impaired apoptosis of the T- lymphocytes. It could be concluded
that immunotherapy have a role in skewing the cytokine profile in asthma and
maintain the balance between Th1/Th2.