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)

We have recently reported the isolation of a human immunodeficiency virus type 1 (HIV-1), KB-1gp32 carrying a shorter size (32 kDa) of transmembrane glycoprotein (TMP) from TALL-1 cells persistently infected with KB-1gp41 virus strain (Shimizu et al., 1990a). Endoglycosidase treatments showed that the different size of the TMP between the two strains was due to a truncation of 9 kDa of polypeptide in the KB-1gp32 TMP coding region. Sequence analysis revealed the substitution of a CAG codon to a TAG stop codon just downstream of the putative membrane-spanning domain of the TMP of KB-1gp32. This resulted in a truncation of some 133 amino acids of the cytoplasmic domain of TMP. The data indicate that a premature stop codon in KB-1gp32 has been introduced during adaption of the parental virus to TALL-1 cells. We have constructed two chimeric clones between the env region of a clone pKB-1, derived from KB-1gp32, and an infectious molecular clone pNL-432. We have also constructed a site-directed mutant of pNL-432 carrying a premature stop codon at the same position as the env stop codon of pKB-1. Among the three clones carrying a premature stop codon in env, only one chimeric clone was infectious to TALL-1 but not MT-2 cells. This clone contained the entire tat, rev, vpu, and env genes of pKB-1. The pNL-432 mutant was not infectious. The results suggest that some sequences of pKB-1 might compensate for the truncation of the TMP during replication in TALL-1 cells.
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PMID:Analysis of a human immunodeficiency virus type 1 isolate carrying a truncated transmembrane glycoprotein. 132 87

Persistently HIV-infected cell lines were isolated from surviving and proliferating cells after infection of HTLV-I-carrying MT-4 cells with cell-free human immunodeficiency virus (HIV); HTLV-IIIB and LAV. The media of the cloned cell cultures did not cause HIV infection of MT-4, MOLT-4, TALL-1, or HL-60 cells. Most of the constituents of the virus in the media were env proteins and many defective doughnut-shaped particles released from the cells were identified by electron microscopy.
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PMID:Defective human immunodeficiency virus (HIV) particles produced by cloned cells of HTLV-I-carrying MT-4 cells persistently infected with HIV. 289 63

Two T-cell lines, TALL-1 and CCRF-CEM, were infected with human immunodeficiency virus (HIV), strain LAV, to explore the time course of the appearance of various virus specific antigens, and to establish an antibody assay system by indirect immunofluorescence (IF). These cells were infected with LAV at two different input multiplicity of infection (MOI). Antigens were tested by Western blot analysis (WB) and IF. Antigens for WB were extracted from the infected cells at various times after infection, but pooled sera of American HIV carriers could not recognize gp41 or gp160. Antigen expression was highest in CCRF-CEM, but, as the antigen for IF, TALL-1 infected at the MOI of 8.0 was the most suitable 7 days after infection, because it includes a fairly large number of uninfected cells, which served as the internal control.
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PMID:Replication of human immunodeficiency virus in two T-cell lines and their application as antigens for immunofluorescence. 305 Mar 77

The effect of 3'-azido-3'-deoxythymidine (AZT) on replication of human immunodeficiency virus (HIV) in various hematopoietic cell lines was investigated. The concentration of AZT required to block HIV replication varied depending on the cell line used. U-937 cells required as little as 0.01 microM AZT to block HIV replication, a concentration almost 100 times lower than that required for MT-4 or MOLT-4 cells. However, 467 and TALL-1 cells required concentrations of AZT higher than 5 microM. It was clear that AZT was ineffective once the viral gene was integrated into chromosomal DNA; removal of AZT from culture fluids at that stage allowed the full expression of HIV. The effect of the potent immunostimulator lentinan was also examined, and it was shown that lentinan enhanced the effect of AZT.
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PMID:Suppression of human immunodeficiency virus replication by 3'-azido-3'-deoxythymidine in various human hematopoietic cell lines in vitro: augmentation of the effect by lentinan. 311 74

Liposomes containing fragment A of diphtheria toxin killed human immunodeficiency virus (HIV)-producing MOLT-4 or TALL-1 cells, and HTLV-I-carrying MT-4 cells infected with HIV, but did not kill these cells when they were not infected with HIV. This killing was not affected by the presence of HIV antibodies. These results show that liposomes containing fragment A of diphtheria toxin selectively killed cells expressing HIV antigens or producing the virus in vitro.
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PMID:Selective killing of human immunodeficiency virus-infected and -producing cells by liposomes containing diphtheria toxin fragment A. 312 51

The effect of human natural interferons (IFN) alpha, beta, and gamma on the replication of human immunodeficiency virus (HIV) strain LAV in T cell lines TALL-1 and CCRF-CEM and peripheral blood lymphocytes (PBL) was studied. The growth of TALL-1 was moderately sensitive to these IFN, whereas that of CCRF-CEM was resistant to them. The progeny virus yield of LAV in TALL-1 at the time of its peak was reduced to 10% of the control level at IFN-alpha, beta, and gamma concentrations of 3, 11, and 23 IU/ml, respectively. These concentrations of IFN-alpha, beta, and gamma did not affect the cell growth. In CCRF-CEM, IFN-alpha, beta, and gamma at the concentration of 50, 60, and 76 IU/ml reduced the progeny virus to 10% of the control level. The virus growth in PBL was more sensitive to IFN than that in CCRF-CEM. The progeny virus yield was reduced to 10% of the control level by IFN-alpha and beta concentrations of 5 IU/ml and less than 5 IU/ml, respectively.
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PMID:Inhibition of growth of HIV by human natural interferon in vitro. 314 96

Syncytium formation is one of major cytopathic effects of human immunodeficiency virus (HIV) infection, and requires the interaction of CD4 molecules on uninfected cells with HIV envelope glycoprotein gp120 expressed on HIV-infected cells. Recent evidence suggests chemokine receptors function as fusion cofactors. We have recently found that fusion regulatory protein (FRP)-1/ CD98 is involved in syncytium formation of HIV gp160-expressing U2ME-7 cells and TALL-1 cells persistently infected with HIV. However, resting lymphocytes were found to express no FRP-1 molecule. In this study, we demonstrated that recombinant gp120 (rpg120) has the ability to induce expression of FRP-1 on peripheral blood mononuclear cells (PBMC). Three-color flow cytometric analysis showed that rgp120-induced FRP-1 was expressed selectively on CD4+ T cells in a dose-dependent manner. FRP-1 expression level was maximum 3 days after addition of rgp120. Anti-CD4 and anti-gp120 antibodies blocked rgp120-induced FRP-1 expression. Co-cultivation of PBMC with HIV-1 gp160-expressing HeLa cells also resulted in the increased expression of FRP-1 on T cells. These results suggest that FRP-1 molecules are induced on CD4+ T cells via CD4-gp120 interaction and may play an important role in regulation of HIV-induced syncytium formation.
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PMID:Human immunodeficiency virus type-1 envelope glycoprotein gp120 induces expression of fusion regulatory protein (FRP)-1/CD98 on CD4+ T cells: a possible regulatory mechanism of HIV-induced syncytium formation. 913 96

Maintenance of B-lymphocyte homeostasis requires balanced cell production, death, and proliferation. To coordinate these processes, B cells are dependent on cell extrinsic signals. In lymphocyte development, precursor cells are dependent on Fms-like tyrosine kinase ligand 3 (Flt3L), and pre-B cells are dependent on the cytokine interleukin-7. Transitional B cells require B-lymphocyte stimulator (BLyS) for survival. Mature B cells require B-cell receptor (BCR) signals and also remain sensitive to their microenvironment. An emerging model suggests that extrinsic signals do not regulate B-cell survival through a digital mechanism where cells are simply instructed to survive or die. Instead, availability and competition for extrinsic signals regulates cellular physiology and metabolism in an analog fashion that then influences cell commitment to apoptosis or proliferation. Decreases in cellular metabolism may sensitize cells to activation and action of the pro-apoptotic Bcl-2 family members, Bak and Bax, and promote apoptosis. In contrast, increases in metabolism may predispose cells to proliferate. Analog control of cell physiology can, thus, be integrated with other inputs by individual cells to produce a fate decision for survival, proliferation, or apoptosis and prevent diseases of cell death, such as immunodeficiency, and cell activation and proliferation, such as autoimmunity or cancer.
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PMID:B-cell homeostasis: digital survival or analog growth? 1496 91

Understanding the development of autoimmunity is a crucial step toward improving the management, not only of autoimmune diseases, but also of tumors and primary immunodeficiency syndromes. The rapid expansion of knowledge on autoimmunity is fueling the development of a novel approach known as targeted immunotherapy. The present review will concentrate on ten areas where major advances have been achieved: 1) early regulation of B-cell mediated autoimmunity; 2) thymic regulation of tolerance to tissue-restricted antigens via the transcription factor AIRE; 3) role for a population of regulatory T cells (CD4+ CD25+ Tregs) with unique effects; 4) major role for dendritic cells in the development of autoimmunity in conditions such as lupus; 5) role for T cells in autoimmune diseases; 6) role for T cells in rheumatoid arthritis, with new data from a murine model of spontaneous arthritis related to a ZAP-70 mutation; 7) role for the environment via innate immunity, in particular mediated by the toll-like receptors (TLR); identification of new autoantigens with the description of sense-antisense peptides (e.g., proteinase 3-complementary proteinase 3); the immunosenescence concept, which suggests that some autoimmune diseases may be related to premature aging of the immune system; 10) identification of new immunotherapy targets, including costimulation pathway molecules (CD28, CTLA4), original activation systems (BAFF/BLyS), and receptors such as TLRs. These exciting insights into the pathogenic mechanisms underlying immune dysfunction will play a key role in advancing the field of immunorheumatology.
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PMID:Novel concepts and treatments for autoimmune disease: ten focal points. 1558 31

DeltaBAFF is a novel splicing isoform of the regulator B cell-activating factor (BAFF, BLyS), a TNF family protein with powerful immunoregulatory effects. Overexpression of BAFF leads to excessive B cell accumulation, activation, autoantibodies, and lupus-like disease, whereas an absence of BAFF causes peripheral B cell immunodeficiency. Based on the ability of DeltaBAFF to multimerize with full-length BAFF and to limit BAFF proteolytic shedding from the cell surface, we previously proposed a role for DeltaBAFF in restraining the effects of BAFF and in regulating B lymphocyte homeostasis. To test these ideas we generated mice transgenic for DeltaBAFF under the control of human CD68 regulatory elements, which target expression to myeloid and dendritic cells. We also generated in parallel BAFF transgenic mice using the same expression elements. Analysis of the transgenic mice revealed that DeltaBAFF and BAFF had opposing effects on B cell survival and marginal zone B cell numbers. DeltaBAFF transgenic mice had reduced B cell numbers and T cell-dependent Ab responses, but normal preimmune serum Ig levels. In contrast, BAFF transgenic mice had extraordinarily elevated Ig levels and increases in subsets of B cells. Unexpectedly, both BAFF and DeltaBAFF appeared to modulate the numbers of B-1 phenotype B cells.
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PMID:deltaBAFF, a splice isoform of BAFF, opposes full-length BAFF activity in vivo in transgenic mouse models. 1597 64


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