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العنوان
The role of CXCR5+ CD4+T follicular helper
Cells in Idiopathic Thrombocytopenic
Purpura /
المؤلف
El-Sayed, Nada El-Sayed Taha.
هيئة الاعداد
باحث / ندي السيد طه السيد
مشرف / فاطمة محمود غيث
مناقش / محمد رمضان الشنشوري
مناقش / محمد حسني محمد فوده
الموضوع
Clinical Pathology.
تاريخ النشر
2019.
عدد الصفحات
p 110. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
21/7/2019
مكان الإجازة
جامعة طنطا - كلية الطب - Clinical Pathology
الفهرس
Only 14 pages are availabe for public view

from 140

from 140

Abstract

Summary
Primary immune thrombocytopenia (ITP) is an autoimmune
disorder caused by both increased peripheral platelet destruction and
impaired platelet production and is usually characterized by platelet
counts less than 100 × 10 ⁹ /L. It often occurs in children following a
viral or bacterial infection and self-resolves.
Production of autoantibodies against platelet glycoproteins
(GP) and opsonization with these autoantibodies lead to platelet
clearance by the reticuloendothelial system. Autoantibodies
production often occurs due to the loss of self-tolerance and increased
stimulation of the immune system.
Antibody responses are largely dependent on the help provided
by CD4+ T cells.Recently, CD4+ T cells present in B cell follicles,
named T follicular helper (Tfh) cells, which is identified by
expression of the B cell follicle homing receptor CXCR5. Tfh cells
trigger the formation and maintenance of germinal centers through
the expression of CD40 ligand (CD40L) and the secretion of IL-
21 and IL-4.
Tfh cells play a critical role in mediating the selection and
survival of B cells that go on to differentiate either into
special plasma cells capable of producing high affinity antibodies
against foreign antigen, or memory B cells capable of quick immune
re-activation in the future if ever the same antigen is re-encountered.
Autoimmune diseases are caused by a breakdown of immune
tolerance. Proliferation of self-reactive B cells with generation of
high-affinity autoantibodies participate to the pathophysiology of