الفهرس 
Chronic lymphocytic leukemiaOnly 14 pages are availabe for public view
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Abstract
Among all hematological malignancies, chronic lymphocytic leukemia has the
highest heterogeneity in its clinical presentation and course. CLL can emerge as an
aggressive and life threating leukemia or as an indolent form that will not require
intervention over long time. The clinical staging systems for CLL are simple,
noninvasive and inexpensive but not sufficient to predict disease progression and
survival. With increased understanding of molecular pathogenesis, a plethora of novel
molecular and biological markers have reflected the outcome of CLL.
The median age for CLL diagnosis is about 72 years and more males are
affected than females (ratio of 1.7:1). However, there is an increase in discovery of CLL
in younger patients diagnosed with early stage and minimal symptoms due to more
frequent blood testing in routine checkup.
CLL is characterized by the clonal proliferation and accumulation of mature
CD5 positive B cells that circulate back and forward between blood, bone marrow,
lymph nodes and spleen forming pseudofollicles. It is now well established that several
genetic and molecular events are the corner stone in the development of CLL. The
diagnosis of CLL is typically by blood count, blood smear and immunophenotyping of
the circulating peripheral blood lymphocytes.
TLR2 is the receptor for a functional recognition of bacterial lipopeptides and is
upregulated during disorders such as chronic obstructive pulmonary disease and sepsis.
TLR2 is expressed on microglia, intestinal epithelial cells and subsets of lamina propria
mononuclear cells in the gastrointestinal tract, monocytes, macrophages, dendritic cells,
polymorphonuclear leukocytes, B cells and T cells, including CD4+CD25+ regulatory T
cells (Tregs.).
There are three possible mechanisms by which TLRs trigger the pathogenesis of
B cell malignancies. First, they can induce B-cell transformation by increasing the
double stranded DNA breaks after activation of naive B-cells or by enhancing proinflammatory microenvironment that increases incidence mutations. Secondly, TLRs
can inhibit apoptosis through the specific activation of NF-κB. Finally, TLRs
stimulation can modulate the immune response through malignant B-cell.
Our study has been conducted to evaluate TLR2%expression in peripheral blood
in CLL patients and to correlate them to different patient‘s characteristics.
The study included 40 subjects. Twenty one typical CLL patients and nineteen
age and sex matched normal controls. The diagnosis of CLL was confirmed by
immunophenotyping scoring system of CLL.
All patients were subjected to the followings: Full history taking and clinical
examination, chest, abdominal and pelvic C.T scan and laboratory
investigations which include CBC and blood film, LDH ,ESR and β2
microglobulin levels and routine immunophenotyping. In addition toTLR2% expression
analysis by flowcytometry
This study has shown that TLR2% expression was significantly higher on B
lymphocytes in patients with CLL compared with controls and also demonstratedSummary
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statistically significant association between TLR2 and splenomegaly.No significant
association between TLR2% and other clinical and laboratory characteristics of patients.