کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5592132 | 1570706 | 2017 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CD11b regulates antibody class switching via induction of AID
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کلمات کلیدی
SHMB cell receptorsTfh cellFollicular helper T cellITGAMactivation induced cytidine deaminaseCFSEActivation-induced cytidine deaminaseCD11BTLRBCRCSRNF-κBsomatic hypermutation - ابرمتن سوتیclass switch recombination - بازوی سوئیچ کلاسclass switching - تعویض کلاسToll-like receptor - تیالآرSystemic lupus erythematosus - لوپوس اریتماتوی سیستمیکSLE - لوپوس منتشر یا لوپوس اریتماتوس سیستمیکGerminal center - مرکز ژرمینالAntibody - پادتَن یا آنتیبادیcarboxyfluorescein succinimidyl ester - کربوکسیفلوورسسین سوکسینیمیدیل استرAID - کمک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The integrin CD11b, which is encoded by the integrin subunit alpha M (ITGAM), is primarily expressed on the surface of innate immune cells. Genetic variations in ITGAM are among the strongest risk factors for systemic lupus erythematosus, an autoimmune disease characterized by the presence of autoantibodies. However, the regulatory function of CD11b in the antibody responses remains unclear. Here, we report the induction of CD11b in activated B2 B cells and define its unexpected role in immunoglobulin heavy chain class switch recombination (CSR). LPS-activated B cells lacking CD11b yielded fewer IgG subtypes such as IgG1 and IgG2a in vitro, and immunization-dependent CSR and affinity maturation of antibodies were severely impaired in CD11b-deficient mice. Notably, we observed the reduced expression of activation-induced cytidine deaminase (AID), an enzyme that initiates CSR and somatic hypermutation, and ectopic expression of AID was sufficient to rescue the defective CSR of CD11b-deficient B cells. LPS-induced phosphorylation of NF-κB p65 and IκBα was attenuated in CD11b-deficient B cells, and hyperactivation of IκB kinase 2 restored the defective AID expression and CSR, which implied that CD11b regulates the NF-κB-dependent induction of AID. Overall, our experimental evidence emphasized the function of CD11b in antibody responses and the role of CD11b as a vital regulator of CSR.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 87, July 2017, Pages 47-59
Journal: Molecular Immunology - Volume 87, July 2017, Pages 47-59
نویسندگان
Seohyun Park, Hyunsub Sim, Hye-In Kim, Daecheol Jeong, Guang Wu, Soo Young Cho, Young Seek Lee, Hyung-Joo Kwon, Keunwook Lee,