Showing papers by "Elaine F. Reed published in 2004"
TL;DR: Exposure of the graft endothelium to low concentrations of anti-HLA Ab may promote cell survival by transducing signals resulting in upregulation of cell survival genes.
120 citations
TL;DR: Larger studies are needed to identify other class II major histocompatibility complex alleles that may influence disease predisposition, disease severity, or both, to ultimately illuminate the regulatory effects of these alleles in the predisposition and severity of RRP.
65 citations
TL;DR: This study is the first to identify a possible association between HLA-DRB1*0404 and VKH disease, as well as to find DRB 1*0102 and DRB1-0410 in Mestizo patients.
44 citations
TL;DR: It is shown that class I ligation results in activation of Rho and increased stress fiber formation, which suggests that HLA class I-induced signaling in EC is dependent on Rho GTPase and ROK.
39 citations
TL;DR: The data do not support the previous suggestion that the HLA-A29.1 serotype may be protective against development of birdshot retinochoroidopathy and additional studies will be required to determine whether the other, less common subtypes are associated with the disease.
36 citations
TL;DR: Increased responses in individuals with HLA class II genotypes that predispose to SLE suggest that peptide presentation by those molecules permits brisker peripheral blood cell responses to autoantibody peptides, thus increasing risk for disease.
Abstract: Peptides from VH regions of antibodies to DNA drive immune responses in systemic lupus erythematosus (SLE). We studied peptide-induced cytokine release by peripheral blood mononuclear cells (PBMC) of patients, the influence of peptide concentration, disease characteristics and HLA-D haplotypes. Cells secreting cytokines (IFNg, IL-2, IL-4 and IL-10) were measured by ELISPOT in PBMC from 31 patients with SLE and 20 matched healthy controls in response to seven peptides (A-G) from the CDR1/FR2 to CDR2/FR3 VH regions of human anti-DNA MAbs. Disease activity was assessed by SELENA-SLEDAI. HLA-DR and -DQ alleles were determined by molecular typing techniques. PBMC from significantly higher proportions of SLE patients than controls responded to VH peptides by generating IFNg and IL-10. Type of cytokines released in response to at least one peptide (D) depended on antigen concentration. Cytokine release was not associated with clinical features of SLE except for disease duration. A shift occurred from IFNg, IL-4 ...
21 citations
TL;DR: In this paper, the authors examined whether a known TAP1 polymorphism in the ATPase domain altered the severity of disease in patients with recurrent respiratory papillomatosis (RRP).
Abstract: Recurrent respiratory papillomatosis (RRP) is a rare disease caused by human papillomaviruses (HPVs). It is characterized by multiple recurrences of benign neoplasms and has a variable clinical course, ranging from infrequent recurrence to acute airway obstruction. One way in which HPV subverts the immune system in RRP is by interfering with TAP1 (transporter associated with antigen presentation 1). We examined whether a known TAP1 polymorphism in the ATPase domain altered the severity of disease in patients with RRP. The presence of this polymorphism was significantly correlated with severity of disease (P = .015). Because of the proximity of the TAP1 gene to human leukocyte antigen (HLA) class II genes on chromosome 6, we postulated that a linkage disequilibrium may exist. Of the patients with polymorphic TAP1, 36% were positive for HLADRB1 ⋆ 0102 (P = .021; P = .147 with Bonferroni's correction). However, this association appeared to mitigate the severity of disease (P = .04). Therefore, severity of disease in a patient with RRP might be determined by sequencing TAP1, in conjunction with HLA class II genes.
19 citations
TL;DR: It is concluded that the present SBT method is a technically simple and robust procedure to characterize the sequence polymorphisms in exon 2 of DQA1 gene.
13 citations
TL;DR: Characterizing the response of endothelial and smooth muscle cells to antigraft antibodies and elucidating the signaling pathways have the potential to identify novel immunotherapies to promote cell survival while preventing transplant arteriosclerosis.
Abstract: Purpose of reviewPatients exhibiting a humoral immune response to the allograft demonstrate a lower graft survival and an increased risk of the development of transplant arteriosclerosis. Unfortunately, current immunosuppressive regimens are not effective in controlling the humoral response to the allograft. This article focuses on the recent progress made toward understanding the role of antigraft antibodies in chronic rejection and graft accommodation. Recent findingsRecent studies suggest that antigraft antibodies play an important role in controlling endothelial and smooth muscle cell homeostasis, in the absence of complement, by binding to ligands on the surface of the cell and transducing intracellular signals. Antigraft antibodies exhibit two primary effector functions: stimulation of cell proliferation and upregulation of cell survival genes. The intracellular events initiated by antibody ligation appear to be influenced by the cell type, specificity, and concentration of the antibody and the degree of molecular aggregation. SummaryCharacterizing the response of endothelial and smooth muscle cells to antigraft antibodies and elucidating the signaling pathways have the potential to identify novel immunotherapies to promote cell survival while preventing transplant arteriosclerosis.
8 citations