The Diagnostic Value of Transcription Factors T-bet/GATA3 Ratio in Predicting Antibody-Mediated Rejection
نویسندگان
چکیده
BACKGROUND Previous data showed that the predominance of intraglomerular T-bet or GATA3 is correlated with different mechanisms of rejection, suggesting that the ratio of T-bet/GATA3 might be used to distinguish antibody-mediated rejection (ABMR) and T-cell-mediated rejection (TCMR). METHODS We compared the intraglomerular T-bet/GATA3 ratio in ABMR and TCMR. The intragraft expression of T-bet and GATA3 was studied via immunohistochemistry. The correlation of the diagnosis of AMR with the ratio of T-bet/GATA3 was examined. RESULTS Both intraglomerular T-bet- and GATA3-expressing cells were increased during acute rejection. T-bet/GATA3>1 was strongly correlated with ABMR (93.3% versus 18.2%). The incidence of positive HLA-I/II antibodies and glomerulitis is significantly higher in T-bet/GATA3>1 group (P < 0.001, 0.013, resp.). The scores of peritubular capillary inflammation and glomerulitis were also higher in T-bet/GATA3>1 group (P = 0.052, P < 0.001, resp.). Nevertheless, T-bet/GATA3>1 is also correlated with C4d-negative ABMR and resistance to steroid treatment. Compared with C4d deposition, T-bet/GATA3>1 had a slight lower (90% versus 100%) specificity but a much higher (87.5% versus 68.8%) sensitivity. CONCLUSION Our data suggested that intraglomerular predominance of T-bet over GATA3 might be used as diagnosis maker of ABMR in addition to C4d, especially in C4d-negative cases.
منابع مشابه
بررسی بیان ژن های T-bet و GATA-3 در کودکان مبتلا به آسم آلرژیک در مقایسه با گروه شاهد
Background and purpose: Allergic asthma is a chronic inflammatory disorder with increased inflammation and bronchial over react to stimulants. Th1 and Th2 cells are the main cells involved in the pathophysiology of asthma. The function of these cells is under the influence of T-bet and GATA3 transcription factors. This study aimed to investigate the impairment of immune responses in patients wi...
متن کاملImmunological Aspect on Late Allograft Dysfunction
Organ transplantation is a well-accepted treatment for patients with end-stage organ failure. Despite continued improvement in short-term graft survival, late allograft dys-function remains a significant problem in the clinic, especially in kidney transplant patients. Many factors contribute to late graft dysfunction, and among them immunological factors are the leading cause of late grafts los...
متن کاملDouble deficiency for RORγt and T-bet drives Th2-mediated allograft rejection in mice.
Although Th1, Th2, and Th17 cells are thought to be major effector cells in adaptive alloimmune responses, their respective contribution to allograft rejection remains unclear. To precisely address this, we used mice genetically modified for the Th1 and Th17 hallmark transcription factors T-bet and RORγt, respectively, which allowed us to study the alloreactive role of each subset in an experim...
متن کاملT-bet and GATA3 orchestrate Th1 and Th2 differentiation through lineage-specific targeting of distal regulatory elements
T-bet and GATA3 regulate the CD4+ T cell Th1/Th2 cell fate decision but little is known about the interplay between these factors outside of the murine Ifng and Il4/Il5/Il13 loci. Here we show that T-bet and GATA3 bind to multiple distal sites at immune regulatory genes in human effector T cells. These sites display markers of functional elements, act as enhancers in reporter assays and are ass...
متن کاملDifferent Expressions of Specific Transcription Factors of Th1 (T-bet) and Th2 cells (GATA-3) by Peripheral Blood Mononuclear Cells From Patients With Multiple Sclerosis
Introduction: Multiple Sclerosis (MS) is an inflammatory disorder caused by self-reactive Th1 lymphocytes, while Th2 cells may confer protection. The Th1 and Th2 cell differentiation are regulated by specific transcription factors, especially T-bet and GATA-3, respectively. This investigation aimed to measure the T-bet and GATA-3 expression by Peripheral Blood Mononuclear Cells (PBMCs) obtained...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
دوره 2013 شماره
صفحات -
تاریخ انتشار 2013