Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Generalized actinomycosis as well as other fungal lesions are typical for children with congenital or acquired immunodeficiencies. The present case of generalized actinomycosis developed against the background of the immunodeficiency resulting from dysplasia of the thymus and lymphoid tissue after chemotherapy of abdominal tumour.
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PMID:[Generalized actinomycosis in an 8-month-old child]. 159 88

The v- and c-Rel oncoproteins bind to oligonucleotides containing kappa B motifs, form heterodimers with other members of the Rel family, and modulate expression of genes linked to kappa B motifs. Here, we report that the RxxRxRxxC motif conserved in all Rel/kappa B family proteins is absolutely required for v-Rel protein-DNA contact and its resulting transforming activity. We also demonstrate that serine substitution of the cysteine residue conserved within this motif enables v-Rel to escape redox control, thereby promoting overall DNA binding. These mutant proteins retained the ability to competitively inhibit kappa B-mediated transcriptional activation of the human immunodeficiency virus long terminal repeat but failed to efficiently transform chicken lymphoid cells both in vitro and in vivo. Our data indicate that reduction of the conserved cysteine residue in the RxxRxRxxC motif may be required for optimal DNA-protein interactions. These results provide direct biochemical evidence that the DNA-binding activity of v-Rel is subject to redox control and that the conserved cysteine residue in the RxxRxRxxC motif is critical for this regulation. These studies suggest that the DNA-binding, transcriptional, and biological activities of Rel family proteins may also be subject to redox control in vivo.
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PMID:The RxxRxRxxC motif conserved in all Rel/kappa B proteins is essential for the DNA-binding activity and redox regulation of the v-Rel oncoprotein. 162 Jan 18

Bone marrow transplant recipients are known to be immunodeficient in cellular and humoral immune responses for months to years. Mechanisms underlying the post-transplant immunodeficiency are mostly unknown and therefore it has been difficult to design therapeutic strategies to address this problem. Here, we review studies of post-transplant B cell (humoral) immunity including B cell blood counts, phenotype, function and origin, and the morphology of lymphoid organs. We postulate that the aetiology of post-transplant humoral immunodeficiency is multifactorial, involving: B cell immaturity due to recapitulation of their ontogenesis, and, in some patients, insufficient T cell help and/or exaggerated CD8+ T cell/NK cell suppression. Implications for clinical practice are outlined, e.g. hypersensitivity reactions and autoimmune diseases as part of the differential diagnosis of post-transplant disorders, questionable diagnostic benefit of serologic studies, and usefulness of prophylactic intravenous immunoglobulin.
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PMID:Reconstitution of B cell immunity following bone marrow transplantation. 162 22

Serum neopterin levels were analysed in 43 patients with primary hypogammaglobulinaemia (25 common variable immunodeficiency (CVI), 12 congenital hypogammaglobulinaemia (CH), six X-linked hypogammaglobulinaemia (XLH)), and in 33 healthy controls. The neopterin values were correlated to lymphocyte subset counts in peripheral blood, lymphocyte mitogen responses and clinical and histological manifestations in the study group. Serum neopterin levels were significantly elevated in all subgroups of patients and particularly in the CVI groups where the highest concentrations were found (P less than 0.001, CVI versus controls). Furthermore, in CVI and CH patients elevated neopterin levels were strongly correlated to decreased number of CD4+ lymphocytes (rs = -0.61, P less than 0.005 and rs = -0.83, P less than 0.001, respectively). In the CVI group high neopterin levels were also significantly correlated to low number of circulatory B (CD19+) lymphocytes (rs = -0.58, P less than 0.05). Both patients with moderately and those with severely depressed lymphocyte mitogen responses had significantly higher neopterin levels than those with normal responses. In addition, high neopterin levels were significantly associated with the occurrence of splenomegaly and nodular intestinal lymphoid hyperplasia. The immunological findings were consistently observed in longitudinal testing, and appeared to be characteristic for the individual patient. High serum neopterin levels are thought to be a marker for hyperactivity in monocytes/macrophages, and dysfunction of these cells may therefore be associated with fundamental immune pathology in some subgroups of primary hypogammaglobulinaemia.
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PMID:Raised serum neopterin levels in patients with primary hypogammaglobulinaemia; correlation to other immunological parameters and to clinical and histological features. 163 65

Infectious bursal disease (IBD) is a highly contagious disease of young chickens, which occurs world-wide, and is responsible for severe losses in poultry industries. In birds surviving an acute infection, lymphoid cells in the bursa of Fabricius are destroyed, resulting in B-cell-dependent immunodeficiency. This causes increased susceptibility to diseases by otherwise harmless agents. The decisive role in the pathogenesis of IBD is played by the bursa, representing the target organ of the aetiological agent, infectious bursal disease virus (IBDV). By adaptation of IBDV to chicken embryo cells, we obtained several variants of a pathogenic wild type strain. These variants had altered abilities for replication in actively dividing B lymphocytes and, consequently, had altered pathogenic properties. An IBDV isolate from turkeys, non-pathogenic for chickens, was used to create reassortant virus strains. The virological and the biological characterization of these IBDV variants is reported.
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PMID:[Effect of viral structure and replication characteristics on the pathogenesis of infectious bursal disease]. 164 47

We investigated the clinical, immunologic, and imaging features of parotid enlargement in 10 children seropositive for human immunodeficiency virus (HIV) who were infected prenatally. In seven patients, sonography revealed many small hypoechoic areas suggestive of lymphoid infiltration. In three older children, large anechoic areas suggesting lymphoepithelial cysts were present. The lesions probably represent generalized lymphoid infiltration akin to pulmonary lymphoid hyperplasia, although only two of our patients had radiologic evidence of pulmonary lymphoid hyperplasia. Four of five of the children with parotid enlargement who had immunologic studies were phenotypically HLA-DR5, an immunophenotype associated with improved immune response, occurring in less than one in four in the normal population. This suggests that painless parotid enlargement may be a good prognostic sign in HIV-seropositive children. Parotid enlargement was found in 10 HIV-positive children from 6 months to 11 years old. All except one were infected prenatally.
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PMID:Parotid enlargement in children seropositive for human immunodeficiency virus: imaging findings. 165 45

Double infection of cells by HHV-6, Epstein-Barr virus (EBV) and by human immunodeficiency virus (HIV-1) can enhance viral effects though genetic transactivation. It remained to be clarified, however, by which mechanism different viruses may enter the same cell. We have shown that HHV-6 infection of immature lymphoid cells rigidifies the cytoplasmic membrane and causes receptor proteins for viruses such as CD4 for HIV-1 and CR2 for EBV to be expressed. In our experiments, HHV-6 infected cells were superinfected by HIV1 and caused enhanced cell death. The mechanisms by which receptors were expressed after HHV-6 infection appears independent of cell membrane rigidification alone and is suppressed by cycloheximide only to a certain extent.
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PMID:Human herpesvirus-6 infection may predispose cells to superinfection by other viruses. 165 48

Clonal lines of human rhabdomyosarcoma (RD) cells, constitutively expressing human immunodeficiency virus type 1 (HIV-1) tat gene (RD tat cell lines) showed enhanced expression of human cytomegalovirus (HCMV) immediate-early (IE) and late (L) proteins upon HCMV infection, as compared with control RD cells. One of the RD tat cell lines produced infectious HCMV. The RD-tat cell lines, following transfection with recombinant plasmids containing the full length of the HCMV-IE enhancer/promoter linked to the bacterial chloramphenicol acetyltransferase (CAT) gene, exhibited an increased CAT expression by the tat product. A chronically HIV-1-infected human T-lymphoid cell line, SupT1, superinfected with HCMV, expressed HCMV-IE proteins while the parental SupT1 cells infected with HCMV were negative. Parental SupT1 cells coinfected with HIV-1 and HCMV also expressed HCMV-IE proteins, indicating that HIV-1-encoded proteins exert a positive regulatory effect on HCMV expression.
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PMID:Human immunodeficiency virus type 1 tat gene enhances human cytomegalovirus gene expression and viral replication. 165 75

Injection of RadLV-Rs viral complex to C57BL/6 mice results in massive enlargement of lymphoid organs. The polyclonal T and B populations which proliferate in spleen and lymph nodes display severely impaired immune functions. Several data suggest that development of this immunodeficiency syndrome is dependent on the presence of T cells whose functions are progressively altered. In contrast, the erythro-myeloid populations and the stem cell compartment are not deeply modified, suggesting that the production of the lymphokines involved in their regulation is not altered. Interleukin 3 (IL-3) is mainly involved in this regulation. Thus, the purpose of the present experiment was to evaluate the IL-3 production: in RadLV-Rs injected mice IL-3 production is decreased at the cellular level but if it is evaluated by taking into account the increase of spleen cellularity, it is initially decreased and later on, above the normal value.
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PMID:Production of interleukin 3 by spleen cells in immunodeficient C57BL/6 mice after injection of RadLV-Rs viral complex. 165 37

Early studies with the Gross passage A leukemia virus demonstrated that retroviral infection suppresses cellular and humoral immune responses. In extensive studies of the feline leukemia (FeLV) virus, which can induce profound immunodeficiency disease, are generative anemia and lymphoid, myeloid and erythroid neoplasia, the immunosuppressive effects of this retrovirus could be attributed to the actions of the retroviral envelope protein p15E. We found that a highly conserved, synthetic 17 amino acid peptide synthesized by Cianciolo and co-workers that is homologous to the hydrophilic portion of the otherwise hydrophobic transmembrane envelope protein can suppress polyclonal activation of B-cells, impair production of gamma- and alpha-interferon, inhibit production of interleukin-2, inhibit expression of IL-2 receptors, and suppress responses of cytotoxic lymphocytes. In analyses with inactivated preparations of the human immunodeficiency virus, with Pahwa et al. we demonstrated that purified non-infectious retrovirus and also retroviral proteins, in particular gp120, appeared to produce some of the immunosuppressive properties of HIV, particularly suppression of B-cell activation in response to known B-cell stimulants irrespective of T-cell influence, suppression of T-helper cell functions essential to B-lymphocyte responsiveness, and impaired function of immunoglobulin-secreting cells. Other investigators have also reported strong immunosuppressive or immunostimulatory influences for components of the HIV retrovirus and also gp120 through yet poorly elucidated but certainly complex actions on both T- and B-lymphocyte-mediated immune functions.
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PMID:In vitro immunomodulation and in vivo immunotherapy of retrovirus-induced immunosuppression. 166 53


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