Predictive factors and impact of full donor T-cell chimerism after reduced intensity conditioning allogeneic stem cell transplantation

This study investigated the kinetics of CD3+-T cell chimerism (TCC) in 102 patients receiving reduced intensity conditioning allogeneic stem cell transplantation (RIC-allo-SCT) from an HLA-identical sibling. Patients with full donor TCC at day 30 had a higher incidence of grade 2–4 acute GVHD compared to patients in mixed TCC (cumulative-incidence, 61% vs. 35%; p=0.01). The delayed establishment of full donor TCC in myeloid malignancies was associated with a higher incidence of relapse (40% vs. 0; p=0.002), suggesting that monitoring of the kinetics of TCC is mandatory after RIC-allo-SCT

Response to Treatment and Disease Progression Linked to CD4+ T Cell Surface CC Chemokine Receptor 5 Density in Human Immunodeficiency Virus Type 1 Vertical Infection

The factors governing interindividual variability in disease progression among children vertically infected with human immunodeficiency virus type 1 (HIV-1) remain unclear. Because it has recently been shown in infected adults that the density of CC chemokine receptor 5 (CCR5) molecules at the surface of nonactivated (human leukocyte antigen [HLA]-DR-) CD4+ T cells correlates with disease progression, the same correlation was sought in children. HLA-DR-CD4+ T cell surface CCR5 density was constant over time and correlated with the bioclinical stage and with the CD4 cell slope observed before antiretroviral treatment. In addition, CCR5 density was negatively correlated with the intensity of the decrease in viremia during antiretroviral therapy and was positively correlated with CD4 cell slope since birth. These results are compatible with the hypothesis that CCR5 density is a key factor governing disease progression in pediatric HIV-1 infection and, thereby, an indicator of prognosis. Moreover, they suggest that therapies aimed at reducing CCR5 accessibility should slow down HIV disease evolution in childre

Spatial and temporal homogeneity of T-cell receptor gamma chain rearrangements in mycosis fungoides: A next-generation sequencing analysis

International audienc

Polymorphism of HLA-DMA and DMB Alleles in Patients with Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease affecting multiple organs that is characterized by the production of various antibodies against nuclear, cytoplasmic, and cell surface antigens. The expression of SLE is influenced by environmental factors and genetic predisposition 1 . Case-control studies have shown that HLA-DR2 and DR3 alleles are associated with SLE 2-5 . HLA class II regions also contain HLA-DMA and HLA-DMB genes. These 2 genes encode respectively for α and ß glycoproteins that make up the HLA-DM heterodimer involved in class II-dependent antigen presentation. To date, 4 DMAalleles and 6 DMB alleles have been described MATERIALAND METHODS Patients and controls. Seventy-three SLE patients (68 women, 5 men, median age 35 yrs, range 12-81) were examined. SLE was diagnosed by 2 rheumatologists according to the American College of Rheumatology (ACR) 1982 revised criteria 14 . All patients were of Caucasian origin. Blood was collected at the Rheumatology Department of the University Hospital of Montpellier. Two unrelated control populations were used in this study. All were healthy volunteer bone marrow donors recruited in the Montpellier area. One group consisted of 147 individuals randomly selected and typed for HLA-DR and HLA-DM genes. To determine if the association between SLE and certain HLA-DM alleles resulted from a direct influence of the DM genes or an indirect influence through linkage disequilibrium with alleles of the DRB1 locus, a second group of controls was defined. This group was composed of 86 individuals carrying DRB1*02 or DRB1*03, the SLE-associated HLA-DRB1 alleles. Methods. Genomic DNAwas extracted from peripheral blood mononuclear cells according to the classic salting-out procedure. DRB1 alleles were typed as describe

Response to treatment and disease progression linked to CD4+ T cell surface CC chemokine receptor 5 density in human immunodeficiency virus type 1 vertical infection

The factors governing interindividual variability in disease progression among children vertically infected with human immunodeficiency virus type 1 (HIV-1) remain unclear. Because it has recently been shown in infected adults that the density of CC chemokine receptor 5 (CCR5) molecules at the surface of nonactivated (human leukocyte antigen [HLA]-DR(-)) CD4+ T cells correlates with disease progression, the same correlation was sought in children. HLA-DR(-)CD4+ T cell surface CCR5 density was constant over time and correlated with the bioclinical stage and with the CD4 cell slope observed before antiretroviral treatment. In addition, CCR5 density was negatively correlated with the intensity of the decrease in viremia during antiretroviral therapy and was positively correlated with CD4 cell slope since birth. These results are compatible with the hypothesis that CCR5 density is a key factor governing disease progression in pediatric HIV-1 infection and, thereby, an indicator of prognosis. Moreover, they suggest that therapies aimed at reducing CCR5 accessibility should slow down HIV disease evolution in children