The clinical and diagnostic relevance of CD23 expression in the chronic lymphoproliferative disease

Abstract

Antiretroviral toxic neuropathy is the most common neurological complication of human immunodeficiency virus infection. This painful neuropathy not only affects the quality of life of human immunodeficiency virus–infected patients but also severely limits viral suppression strategies. We have developed an in vitro model of this toxic neuropathy to better understand the mechanism of neurotoxicity and to test potential neuroprotective compounds. We show that among the dideoxynucleosides, ddC appears to be the most neurotoxic, followed by ddI and then d4T. This reflects their potency in causing neuropathy. AZT, which does not cause a peripheral neuropathy in patients, does not cause significant neurotoxicity in our model. Furthermore, in this model, we show that the immunophilin ligand FK506 but not cyclosporin A prevents the development of neurotoxicity by ddC, as judged by amelioration of ddC‐induced “neuritic pruning,” neuronal mitochondrial depolarization, and neuronal necrotic death. This finding suggests a calcineurin‐independent mechanism of neuroprotection. As calcineurin inhibition underlies the immunosuppressive properties of these clinically used immunophilin ligands, this holds promise for the neuroprotective efficacy of nonimmunosuppressive analogs of FK506 in the prevention or treatment of antiretroviral toxic neuropathy. Ann Neurol 2003;53:000–000

Prognostic impact of p27KIP1 expression in cyclin D1 positive lymphoproliferative disorders

“…CD23 dim positivity has already been reported in MCL. 45,46 Even if its expression appeared more frequent in the non-nodal group, it was always dim and significantly lower than that observed in CLL. Although median survival appeared longer in the nonnodal group (41 months) than in the nodal group (29 months), the overall survival was not significantly different by univariate analysis, nor was it selected by multivariate analysis.…”

Flow cytometric immunophenotyping for hematologic neoplasms

“…26 B-cell lymphoid neoplasms with a CD5 ϩ , CD10 Ϫ phenotype that differs from the typical phenotype of CLL/SLL are more difficult to classify using flow cytometric studies. [27][28][29][30] Although variant phenotypes have been described in CLL/SLL (eg, brighter intensity CD20, brighter intensity surface immunoglobulin, weaker or absent CD23, and expression of FMC-7), additional work-up is generally required to exclude other CD5 ϩ B-cell lymphoid neoplasms. 30 MCL usually demonstrates a CD5 ϩ phenotype that differs from typical CLL/SLL: CD20 moderate to bright intensity, surface For personal use only.…”

The cut‐off levels of CD23 expression in the differential diagnosis of MCL and CLL

“…In flow cytometric practice, CD23 has been widely used as a marker in the differential diagnosis of CLL versus MCL; however, several lines of evidence suggest that the absence or presence of CD23 in a CD19/CD5 cell population fails to faithfully distinguish the two entities. CD23 negativity may occur in CLL [6,7], and in some MCL cases CD23 expression was observed [6,[8][9][10][11]. Differential diagnosis of CLL and MCL is further complicated by the fact that the number of CD23-positive cells and the intensity of CD23 expression may vary in both diseases [6].…”