There are promising data suggesting that it may also have a direct neuroprotective property independent of peripheral lymphocytopenia.<b>Areas covered</b>: We reviewed the pharmacology and the clinical and radiological effects of siponimod.<b>Expert opinion</b>: The selective effect of siponimod on the S1P1 and S1P5 receptors offers a favorable side-effect profile and transient bradycardia can be avoided by dose titration.
B-cell lineage-specific deletion of the GR (glucocorticoid receptor) in CD19-Cre loxP Nr3c1 mice attenuated lymphocytopenia after transient middle cerebral artery.
WDR1 deficiency was associated with even more severe abnormalities of the B-cell compartment, including peripheral B-cell lymphopenia, paucity of B-cell progenitors in the bone marrow, lack of switched memory B cells, reduced clonal diversity, abnormal B-cell spreading, and increased apoptosis on B-cell receptor/Toll-like receptor stimulation.
As mutations in polycystin-1 and -2 are associated with decreased proliferation of immortalized lymphoblastoid cells in PKD, we investigated whether lymphopenia could be an unrecognized trait of PKD.
We have previously shown that mice with generalized ablation of growth hormone (GH) releasing hormone (GHRH) gene (<i>Ghrh</i><sup>-/-</sup>) have normal thymus and T-cell development, but present a marked spleen atrophy and B-cell lymphopenia.
In the pSS group, anaemia (<i>p</i> = 0.0085), lymphocytopenia (<i>p</i> = 0.0006), elevated ERS (<i>p</i> = 0.001), higher RF titer, and ANA antibodies were noted.
In this study, we show that CBLB, a negative regulator of TCR signaling, suppresses CD8<sup>+</sup> T cells in response to inactivated fungal vaccination in a mouse model of CD4<sup>+</sup> T cell lymphopenia.
RAS guanyl-releasing protein 1 (RASGRP1) deficiency has recently been shown to cause a primary immunodeficiency (PID) characterized by CD4<sup>+</sup> T cell lymphopenia and Epstein-Barr virus (EBV)-associated B cell lymphoma.
These studies reveal a new clinical entity of a primary immunodeficiency with T-cell lymphopenia that is associated with compound heterozygous TYK2 mutations in the patients.
Mouse model expressing kinase-dead ATR (Atr<sup>+/KD</sup>), but not loss of ATR (Atr<sup>+/-</sup>), displays ssDNA-dependent defects at the non-homologous region of X-Y chromosomes during male meiosis leading to sterility, and at telomeres, rDNA, and fragile sites during mitosis leading to lymphocytopenia.
Mb1-aPIK3CD mice exhibited bone marrow B lymphopenia and, conversely, expansion of the peripheral innate B1a and MZ B cell compartments. aPIK3CD B cells manifest increased pS6 and increased survival at several stages, without alterations in cycling, and baseline increases in plasma cells, natural IgM, and IgG3.
We have previously shown that mice with generalized ablation of growth hormone (GH) releasing hormone (GHRH) gene (<i>Ghrh</i><sup>-/-</sup>) have normal thymus and T-cell development, but present a marked spleen atrophy and B-cell lymphopenia.
Using both ubiquitous and hematopoietic-specific deletion strategies, the loss of Setd1b resulted in peripheral thrombo- and lymphocytopenia, multilineage dysplasia, myeloid-biased extramedullary hematopoiesis in the spleen, and lethality.
This approach will fail to identify VODI patients because the disease is not associated with severe T cell lymphopenia at birth; (2) the SP110 gene contains 17 exons, making it a challenge for Sanger sequencing.
We found that although BCL-2 and BCL-XL were dispensable for TEC homeostasis, MCL-1 deficiency impacted on TECs as early as embryonic day 15.5, resulting in early thymic atrophy and T-cell lymphopenia, with near complete loss of thymic tissue by 2 months of age.
Sphingosine-1-phosphate (S1P) receptor antagonist and sphingosine kinase 1 (SK1) inhibitor FTY720 (FTY) has promising anticancer properties, however, it causes systemic lymphopenia which impairs its use in cancer patients.
In patients with PMR, B-cell lymphopenia and abnormal B-cell subset distribution are associated with disease activity and IL-6 concentration, and both are corrected by the IL-6 antagonist tocilizumab.