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العنوان
Some Immunological Studies in Tuberculous Patients /
الناشر
Amal Mahmoud Kamal EL-Din,
المؤلف
Kamal EL-Din, Amal Mahmoud.
هيئة الاعداد
باحث / Amal Mahmoud Kamal EL-Din
مشرف / Zeinab Ahmed Ismail
مشرف / Farha Abd EL-Aziz EL-Shinnawy
مشرف / Esmat Abd EL-Aziz EL-Sharkawi
الموضوع
Clinical Pathology. Tuberculous Patients.
تاريخ النشر
2002 .
عدد الصفحات
186 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/1/2002
مكان الإجازة
جامعة المنيا - كلية الطب - الباثولوجيا الإكلينكية
الفهرس
Only 14 pages are availabe for public view

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Abstract

The aim of the work is:
1- Studying the changes in peripheral blood lymphocyte populations occurring in tuberculos patients.
2- Studying the relationship between CD4+ and CD8+ T cells numbers in defense against tuberculoses infection.
3- Measuring the changes in IL-2, IL-4 and IL-8 in the serum and in the supernatant of lymphocyte culture.
4- Evaluating the T-cell mediated immunity in-vitro, by measuring the proliferative responses of peripheral blood mononuclear cells (PBMNC) to non specific stimulant: phytohaemagglutinin (PHA) mitogen.
The following can be concluded from this study:
1- Cellular immunity is central to the outcome of Mycobacterium tuberculosis infection, both phagocytes and Mycobacterium tuberculosis specific T lymphocyte and its products (cytokines), especially those of Th1 and Th2 and Tc1 play a crucial role in this host response. Mycobacterium tuberculosis is one of the pathogens which have the ability to circumvent this first line of defense, therefore thrive within several tissues, even in professional phagocytic cell.
2- The patients with pulmonary tuberculosis have no notable alteration in their total peripheral blood lymphocyte count. This finding together with depressed number of circulating CD4 and increased number of circulating CD8 with normal proliferation response merits further investigations to clarify the precise phenotype of T-cell subset involved.
3- Cellular immune defect is suggested possibly at the level of release of inflammatory cytokines, and may be resulting from the difference in the proportion of CD4.