الفهرس 
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Abstract
The proliferation of monoclonal or polyclonal lymphoid cells in the context of immunological failure characterizes a diverse group of illnesses known as lymphoproliferative disorders (LPD). True malignancy is much more likely to occur in immunocompromised people than in immunocompetent ones.
The blood cancer known as acute lymphoblastic leukemia (ALL) mostly strikes youngsters, however it can also strike adults. This occurs when lymphoid precursor cells proliferate malignantly, invading the bone marrow and perhaps spreading to locations outside of the tumor itself.
The role of antigen presenting cell-expressed CD80 and CD86 in costimulation of T lymphocytes through CD28 ligation is well-established. Furthermore, both ligands have the ability to bind to CTLA-4, an inhibitory receptor that is crucial for controlling T cell responses.
As valuable markers for considering and managing ALL, CD86 and CD80 expressions show substantial promise. Their potential to enhance diagnosis, forecast chemotherapy response, and direct treatment tactics for this difficult disease is one of their many promising therapeutic applications that are now under intense investigation.
The clinical course of chronic lymphocytic leukemia (CLL) demonstrates significant variation. Clinical outcome, responsiveness to treatment, and prognosis can be better predicted by analyzing its clinicohematological and cytogenetic characteristics. Because many individuals do not respond to standard treatment, 17p deletion is recognized as an indicator of a bad prognosis in this setting.
Patient and Method :
The study included 57 lymphoproliferative disorder patients who were admitted to both of Oncology department and pediatric department.
I. Patients:
The patients included in the study were divided as follows:
1. group I: it included 19 patients diagnosed with ALL
2. group II: it included 19 patients diagnosed with CLL
3. group III: it included 19 patients diagnosed with NHL
All patients involved in the study have been subjected to full medical history , examination and routine laboratory investigations were done
C) Routine investigations:
Included complete blood count (CBC) with differential count, LDH, Bone marrow examination , immunophenotyoing.
D) Special investigations:
3- Percentage of expression of CD80 and CD86 on mononuclear cells by Flow cytometry (BD FACS canto II USA).
4- 17p deletion by FISH.
Results of this study were summarized as follow :
In terms of ALL, we discovered that LDH significantly decreased after therapy compared to pre-treatment levels, and both CD86% and CD80% also decreased after treatment compared to pre-treatment levels.
A statistically significant reduction in CD86 and CD80% was observed in both NHL and CLL patients following treatment, as compared to expression levels prior to treatment.
Patients with positive 17P deletion had a significantly higher CD80% (before therapy) compared to patients without this deletion, when looking at subgroups of CLL.
Patients who tested positive for 17P deletion had a significantly higher CD86 (pre-treatment) than those who tested negative for the deletion.
Patients with positive 17P deletion had a statistically significant increase in CD80% (after therapy) compared to patients without this loss.
Compared to individuals without a 17P deletion, those with a positive deletion had a statistically significant rise in CD86% (after therapy).
Patients who tested positive for 17P deletion had significantly higher TLC levels (before therapy) than those who tested negative for the deletion.
Patients who tested positive for 17P deletion had significantly higher TLC levels following treatment compared to those who tested negative for the deletion.
Positive 17P deletion was associated with a statistically significant increase in absolute lymphocyte count (before treatment) compared to negative 17P deletion.
Absolute lymphocyte count (after therapy) was significantly higher in patients with positive 17P deletion compared to those without the deletion.
Conclusion:
In conclusion, studying CD86 and CD80 levels in ALL patients shows promise. These molecules could become important tools for physicians. They might help with diagnosing ALL, predicting how well a patient responds to treatment, and deciding on the best course of action.
The use of CD86 and CD80 molecules as markers of proliferation in lymphoproliferative diseases is further supported by our data. Clinical studies suggest that the CD86 molecule may be involved in CLL etiology; patients whose CD86 expression was elevated required treatment before they could get it. It is possible that the CD86 molecule activates and depletes immunological functions, interfering with the immune system of CLL. Therefore, CD86 positive may indicate a worse prognosis for that reason.
However, new, exciting medications may increase the response rate in this high-risk category of CLL patients, allowing for longer EFS and OS intervals.