کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10940952 | 1095535 | 2015 | 33 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Early and late B cell immune responses in lethal and self-cured rodent malaria
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کلمات کلیدی
iRBCsMBCRBCLDA - تخصیص پنهان دیریکلهperitoneal cavity - حفره صفاقیstandard error - خطای استانداردintraperitoneal - داخل صفاقیPERC - دقیقهRoom temperature - دمای اتاقPCs - رایانه های شخصیMemory B cell - سلول B حافظهplasma cells - سلول های پلاسماPlow - شخم زدنfollicular - فولیکولارB lymphocytes - لنفوسیت BMalaria - مالاریاLimiting dilution assay - محدود کردن آزمون رقتSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیGerminal center - مرکز ژرمینالbone marrow - مغز استخوانmarginal zone - منطقه حاشیه ایParasitemia - پارازیتمیImmune response - پاسخ یا واکنش ایمنیpost-infection - پس از عفونتPyl - پیکانoptical density - چگالی نوریred blood cell - گلبول قرمز، اریتروسیتinfected red blood cells - گلبول های قرمز آلوده
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
ICR mice have heterogeneous susceptibility to lethal Plasmodium yoelii yoelii 17XL from the first days of experimental infection as evidenced by the different parasitemia levels and clinical outcomes. This mouse model has revealed specific immune responses on peripheral blood correlating with the infection fate of the animals. To search for immune-markers linked to parasitemia we examined B lymphocytes in organs of the immune system as key effectors of rodent immunity against malaria. To determine changes in immune cellularity fostered by the different prognostic parasitemia we examined B cell subsets in low (<15%) and high (>50%) parasitized mice during the first days of the infection. In the case of surviving mice, we studied the preservation of memory immune response 500 days after the primary P. yoelii challenge. Correlating with the parasitemia level, it was observed an increase in total cellularity of spleen during the first week of infection which remained after 16 months of the infection in surviving animals. B cell subsets were also modified across the different infection fates. Subpopulation as follicular B cells and B-1 cells proportions behaved differently depending on the parasitemia kinetics. In addition, peritoneal cavity cells proliferated in response to high parasitemia. More significantly, P. yoelii -specific memory B cells remained in the spleen 500 days after the primo-infection. This study demonstrates that B cell kinetics is influenced by the different parasitemia courses which are naturally developed within a same strain of untreated mice. We show that high levels of parasitemia at the beginning of infection promote an extremely fast and exacerbate response of several cell populations in spleen and peritoneal cavity that, in addition, do not follow the kinetics observed in peripheral blood. Furthermore, our results describe the longest persistence of memory B cells long time upon a single malaria infection in mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 220, Issue 5, May 2015, Pages 684-691
Journal: Immunobiology - Volume 220, Issue 5, May 2015, Pages 684-691
نویسندگان
Isabel G. Azcárate, Patricia MarÃn-GarcÃa, Susana Pérez-Benavente, Amalia Diez, Antonio Puyet, José M. Bautista,