Regular ArticleHuman T Cell Activation Induces the Expression of a Novel CD45 Isoform That Is Analogous to Murine B220 and Is Associated with Altered O-Glycan Synthesis and Onset of Apoptosis
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Cited by (21)
TCRαβ<sup>+</sup>CD3<sup>+</sup>CD4<sup>−</sup>CD8<sup>−</sup> (double negative) T cells in autoimmunity
2018, Autoimmunity ReviewsCitation Excerpt :As DN T cells from Fas-deficient MRL.lpr mice, cells from ALPS patients abnormally express the B cell antigen B220, an isoform of the CD45 antigen (that used to be referred to as leukocyte common antigen; LCA) [99]. Of note, the B cell marker B220 is alternatively expressed on activated T cells that undergo apoptosis [100]. Furthermore, DN T cells from ALPS patients co-express CD27 and CD28 [101], a characteristic of naïve and central memory T cell subsets that is usually absent in effector T cells [102].
Underexpression and overexpression of Fas and Fas ligand: a double-edged sword
2010, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :A complete blood cell count may reveal anemia, thrombocytopenia, neutropenia, or lymphocytosis. In certain patients with ALPS, especially type Ia, DNT cells may show an increased expression of B-cell–specific CD45R isoform B220, which may improve the specificity of the flow screening assay for abnormal DNT cells.34–36 First-line therapy for ALPS includes systemic, high-dose corticosteroids.
Phenotypic and functional heterogeneity of human memory B cells
2008, Seminars in ImmunologyCitation Excerpt :Understanding the significance of these findings will require to first elucidate the relationship between the expression of B220 and: (1) the different pathways of memory cell development (GC-dependent and -independent); (2) different memory responses (T-dependent and -independent); (3) the division of labor between B220− and B220+ memory cells in terms of their effector functions (both antibody-dependent and -independent) and their relative participation in protective versus autoimmune responses [12]. One particularly intriguing possibility is that B220 expression could be lost during differentiation into resting (long-lived) central memory cells and upregulated during activation and generation of (short-lived) effector memory B cells [32,52–54]. This model would be consistent with the upregulation of B220 observed in activated mouse and human T cells before they undergo apoptosis [54–56].
Sorting out the causes of ALPS
2005, Journal of Pediatrics
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J.J.H.B. and M.R.M. contributed equally to this work.
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Current address and to whom correspondence should be addressed: Arkansas Children's Hospital Research Institute, 1120 Marshall Street, Slot 512-13, Little Rock, AR 72202. Fax: (501) 320-3173. E-mail: [email protected].