The lectin jacalin induces phosphorylation of ERK and JNK in CD4+ T cells

Journal of Leukocyte Biology

Seetha M. Lakshmi Tamma³  Paul Dominguez³  V. S. Kalyanaraman²  Ron R. Modesto³  Savita Pahwa¹ 

[1] North Shore-LIJ Research Institute, Manhasset, New York North Shore-LIJ Research Institute, Manhasset, New York North Shore-LIJ Research Institute, Manhasset, New York;Department of Cell Biology, Advanced Biosciences Laboratories, Inc., Kensington, Maryland; and Department of Cell Biology, Advanced Biosciences Laboratories, Inc., Kensington, Maryland; and Department of Cell Biology, Advanced Biosciences Laboratories, Inc., Kensington, Maryland; andDepartment of Biomedical Sciences, C. W. Post Campus, Long Island University, Brookville, New York; Department of Biomedical Sciences, C. W. Post Campus, Long Island University, Brookville, New York; Department of Biomedical Sciences, C. W. Post Campus, Long Island University, Brookville, New York;

关键词: PLC-γ1;    vav;    RAS;   

DOI  :  10.1189/jlb.1102534

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

The CD4 molecule plays an essential role in mediating the transduction of intracellular signals by functioning as a coreceptor for the complex T cell receptor/CD3 and also acts as the primary receptor for human immunodeficiency virus (HIV). Several authors have shown evidence that jacalin, a plant lectin, binds to CD4 and inhibits in vitro HIV infection. We analyzed jacalin-induced intracellular signaling events in CD4+ T cells and have shown that cell activation resulted in tyrosine phosphorylation of intracellular substrates p56lck, p59fyn, ZAP-70, p95 vav, phospholipase C-γ1, and ras activation, as assessed by conversion of ras guanosine 5′-diphosphate to ras guanosine 5′-triphosphate. We further examined extracellular regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) phosphorylation following stimulation with jacalin. The data indicate that the kinetics of JNK phosphorylation is delayed. Optimum phosphorylation of ERK2 was observed by 10 min, and that of JNK was observed by 30 min. Pretreatment with gp120 followed by stimulation with jacalin resulted in marked inhibition of all of the aforementioned intracellular events. The data presented here provide insight into the intracellular signaling events associated with the CD4 molecule–jacalin–gp120 interactions and HIV-induced CD4+ T cell anergy. Jacalin may be used as a possible tool for the study of CD4-mediated signal transduction and HIV-impaired CD4+ T cell activation.

【 授权许可】

Unknown