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Blood, 11 June 2009, Vol. 113, No. 24, pp. 6128-6137. Prepublished online as a Blood First Edition Paper on February 3, 2009; DOI 10.1182/blood-2008-10-182329.
Submitted October 2, 2008
Red Cell Physiology Laboratory, New York Blood Center, New York, NY, United States * Corresponding author; email: xan{at}nybloodcenter.org.
Protein 4.1R (4.1R) was first identified in red cells where it plays an important role in maintaining mechanical stability of red cell membrane. 4.1R has also been shown to be expressed in T cells but its function has been unclear. In the present study, we use 4.1R deficient mice to explore the role of 4.1R in T cells. We show that 4.1R is recruited to the immunological synapse following TCR stimulation. We further show that CD4+ T cells of 4.1R-/- mice are hyper-activated and that they displayed hyper-proliferation and increased production of IL-2 and INF
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| Copyright © 2009 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
. The hyper-activation results from enhanced phosphorylation of LAT and its downstream signaling molecule ERK. The 4.1R exerts its effect by binding directly to LAT, and thereby inhibiting its phosphorylation by ZAP-70. Moreover, mice deficient in 4.1R display an elevated humoral response to immunization with T-cell-dependent antigen. Thus, we have defined a hitherto unrecognized role for 4.1R in negatively regulating T cell activation by modulating intracellular signal transduction.
