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

The in vitro maturation of peripheral blood monocytes to macrophages can be followed morphologically, and by measurement of cell surface antigens (CD4, HLA-DR, and FcR III) and lysozyme production. We used these markers to correlate monocyte maturation with susceptibility to human immunodeficiency virus (HIV) infection. Maturation of peripheral blood monocytes is associated with a decrease in membrane CD4, while HLA-DR and FcR III expression increase along with lysozyme secretion. Cells at all stages of maturation were susceptible to HIV infection, even mature macrophages without CD4 detectably by immunofluorescent staining. Maximal replication was observed in 7-day-old cells.
 ...
PMID:Characterization of the in vitro maturation of monocytes and the susceptibility to HIV infection. 169 73

Astrocytes are regarded as matrix of the neuron in central nervous system (CNS) and involve nutritional and supporting function of neuron. It was clarified that human and murine cultured astrocytes had Fc receptor (FcR) on their cell surface from the study of EA rosette assay, reverse ADCC (antibody dependent cellular cytotoxicity) and flow cytometric analysis with anti-FcR monoclonal antibodies (mAb) in this study. Human glioma cells express FcR III recognized by mAb MG 12 and mouse astrocytes express FcR II recognized by mAb 2.4 G 2. Expression of FcR on human astrocytes is compatible with FcR-mediated human immunodeficiency virus (HIV)-1 infection in CNS. Expression of adhesion molecules engaged in T and natural killer cell cytotoxicity was also investigated for human glioma cells. CD 56 (NKH-1 or Leu 19), which is an isoform of N-CAM (neural cell adhesion molecule) mainly distributed on human NK cells and a subset of T cells, was also expressed in neuroglial cells. LFA-3, a ligand for CD 2, but not ICAM-1, a ligand for LFA-1, was, expressed on glioma cells. So, CD 56 was suggested to be a new adhesion molecule in NK cell mediated lysis of glioma cells by their homotypic adhesive character.
 ...
PMID:[Analysis of receptor expression on astrocytic cells]. 170 27

Fc gamma RIII on neutrophils is a phosphatidyl inositol glycan (PIG)-anchored protein that can be released from the cells by activation with chemotactic peptides. We have examined the expression of Fc gamma RIII (CD16), CD11b, and Fc gamma RII (CD32) on neutrophils from human immunodeficiency virus (HIV)-I-infected individuals by two-color FACS. In patients with AIDS and AIDS-related complex and in HIV-I positive intravenous drug abusers we observed a substantial population (25%) of neutrophils that were autofluorescent, and did not stain with the anti-Fc gamma RIII mAb 3G8. This population was largely absent (3%) in HIV-I negative control individuals. No changes in the expression of Fc gamma RII, CD11b, or another PIG-anchored protein, decay accelerating factor (CD55) on neutrophils, were found. The presence of the Fc gamma RIII negative neutrophil population may be related to altered functions leading to common bacterial infections in advanced AIDS.
 ...
PMID:Change in expression of Fc gamma RIII (CD16) on neutrophils from human immunodeficiency virus-infected individuals. 213 22

We have previously reported that, in long-term renal allograft recipients who receive chronic chemical immunosuppression and who are at risk for late chronic viral infections and virus associated tumors, the percentage of lymphocytes the phenotype of which is Leu-7+/Leu-11(-) (CD16) is markedly and significantly increased compared with that in normal controls. Since this population may lack natural killer (NK) activity and may explain the state of decreased host resistance, we carried out studies in 16 kidney transplant recipients on conventional immunosuppression and 10 age-matched normal controls to further define the phenotype, the morphology, and the NK cell activity of this particular subset. Using two-color flow cytometry analysis we found that the Leu-7+ cell subset comprises two essentially nonoverlapping subpopulations, depending on whether cells are coexpressing the NK cell marker Leu-11/CD16 (Leu-7+/Leu-11+ phenotype) or the pan-T cell marker Leu-4/CD3 (Leu-7+/Leu-4+ phenotype). We thus demonstrated that Leu-7+/Leu-11- cells do coexpress the Leu-4+/CD3 surface determinant. The percentage of Leu-7+/Leu-4+ (CD3) is significantly elevated in transplant recipients compared with that in normal controls (26 +/- 4% versus 8 +/- 2%, P less than 0.005). In contrast, the size of the Leu-7+/Leu-11+ cell subset is similar in both groups. Although in transplant recipients 70% of Leu-7+ cells coexpress Leu-4/CD3, only 43% do so in the control group. Cell sorter experiments isolated the Leu-7+/Leu-4+ cells and showed that morphologically these cells are typical large granular lymphocytes that cannot be distinguished from Leu-11+ NK cells. NK-sensitive K562 target cells showed no cytotoxicity. In contrast, Leu-7+/Leu-11+ cells exhibited high killing activity. Therefore, in long-term stable renal allograft recipients at increased risk of developing cancers and chronic viral infections, a subpopulation of non-NK large granular lymphocytes, the phenotype of which is Leu-7+/Leu-11-/Leu-4+, is abnormally expanded. This subset likely contributes to the diminished functional attributes of the chronic drug-induced immunodeficiency.
 ...
PMID:Characterization of an expanded large granular lymphocyte subset lacking natural killer activity present in renal allograft recipients. 243 19

Patients with myeloma have a depressed capacity to respond to antigenic challenge. Studies in this laboratory have previously described an unclassified lymphoid cell which binds human erythrocytes coated with human immunoglobulin G (IgG) anti-D antibody (EA) as important in the inhibition of Ig synthesis in myeloma patients. Using monoclonal antibodies, two-color fluorescence studies, and flow cytometry, we characterized this EA cell as a Leu-1+ (cluster designation (CD) 5), Leu-12+ (CD 19), Leu-16+ (CD 20), B2+ (CD 21), Leu-14+ (CD 22), and HLA-DR+ B cell. The cell was negative for antibodies to Leu-2 (CD 8), Leu-3 (CD 4), Leu-4 (CD 3), Leu-5 (CD 2), Leu-7, Leu-8, Leu-11 (CD 16), Leu-M1 (CD 15), Leu-M3, and CALLA (CD 10). This profile is consistent with a Leu-1+ B cell and excludes a T cell, natural killer cell, and monocyte. Comparison of the relative role of these cells to the role of monocytes in the suppression of pokeweed mitogen-stimulated Ig synthesis was determined in serial studies on 19 myeloma patients. The mean (+/- SEM) percentage of inhibition of Ig synthesis by monocytes from stage I myeloma patients was 14 +/- 2.2%, from stage II patients was 37 +/- 3.5%, and from stage III patients was 51 +/- 4.7%. Inhibition of Ig synthesis by Leu-1+ EA cells was 46 +/- 1.5%, 48 +/- 1.6%, and 43 +/- 3.7% in stage I, II, and III patients, respectively. Immunosuppressive B cells are an important component of inhibition of Ig synthesis in the immunodeficiency of myeloma.
 ...
PMID:Multiple myeloma: an immunologic profile. IV. The EA rosette-forming cell is a Leu-1 positive immunoregulatory B cell. 295 12

A polyclonal T-cell receptor complex (TCR) expression defect (as detected with monoclonal antibody WT31) has been found in two children belonging to an otherwise healthy Spanish family. One of the sibs (V, who had been vaccinated with attenuated poliomyelitis virus) showed clinical signs of immunodeficiency with an autoimmune syndrome, but the other (older) sib (D, vaccinated with attenuated rubella, measles, mumps, and poliomyelitis viruses) has been symptomless throughout life. In contrast to both sibs' normal expression of other peripheral leucocyte markers, as measured by flow cytometry (including CD1, CD2, CD4, CD8, and CD16), only about 6% of CD2+ polyclonal T cells expressed surface antigen-specific T-cell receptor (Ti/WT31), and only about 23% weakly expressed surface CD3 determinants. On the remaining CD2+ T cells in each sib the expression of Ti and CD3 was undetectable; the defect in CD3 expression is very likely secondary to the defect in Ti expression. Natural killer (NK) activity was not increased in any of the sibs, ruling out a high content of NK cells among their CD2+ lymphocytes. Functional data indicate that CD3-mediated T-cell activation with anti-CD3 monoclonals and Ti-mediated responses to allogeneic and tetanus toxoid antigens were severely depressed, whereas activation via CD2 was normal in the T lymphocytes of both sibs. Genes encoding for Ti alpha, beta, and gamma chains did not show major alterations by southern blot analysis, and polyclonal beta chain genes rearrangements were detected in both children's T-cell blasts. Family clustering suggests a genetic pathogenesis, but linkage to HLA or other blood group markers has not been found. Sib V had a concomitant autoimmune disease and died after a severe autoimmune haemolytic anaemia, indicating a relationship between the TCR and generation of autoimmune clones. However, the resistance of both individuals to infection and to vaccination with attenuated viruses, and the fact that sib D has been symptomless to date questions the relative importance of the TCR in the immune response against infection, and suggests that alternative T-cell activation pathways and non-specific defence mechanisms (external surfaces--bound and/or cellular) may suffice under certain circumstances.
 ...
PMID:An in vivo functional immune system lacking polyclonal T-cell surface expression of the CD3/Ti(WT31) complex. 296 74

Antipeptide sera raised against the gp120/gp41 sequences of human immunodeficiency virus type 1 (HIV-1) were used to determine their capacity to enhance infection. Antisera to the five variable regions (V1 to V5) of gp120 and conserved parts of gp120 and gp41 facilitated infection of primary human macrophages with the homologous virus HIV-1 SF2mc. In contrast, heterologous virus infection with HTLV-IIIB was mediated only by antisera to the conserved regions, predominantly C4 and C5. Heterologous virus infection occurred more rapidly and was consistent between different cell donors. The neutralizing monoclonal antibody (MAb) SC258 (murine IgG2a) but not MAb 684-238 (mIgG1) against conformational epitopes of the V2 region also induced antibody-dependent infection enhancement (ADE). Therefore, preincubation with certain antibodies can cause altered tropism of the lymphocytotropic viruses mentioned above. Viral infection was completely abolished by preincubation with the F(ab)2 fragment of MAb 3G8 against the Fc gamma receptor III (CD16). A MAb (7.3F11) against the gp120-binding site of CD4 had no effect on viral infectivity. Possible mechanisms and their implications for disease progression are discussed.
 ...
PMID:Lymphocytotropic strains of HIV type 1 when complexed with enhancing antibodies can infect macrophages via Fc gamma RIII, independently of CD4. 754 Mar 99

A patient with refractory human immunodeficiency virus (HIV)-related immune thrombocytopenic purpura (ITP) was treated with 3G8 (anti-CD16) monoclonal antibody on days 1, 3, and 8 (25, 25, and 50 mg were administered intravenously, respectively). Side effects were those expected after the administration of a xenogenic protein, but a severe bone pain occurred from the second injection. At the time of the initiation of the treatment the platelet count was 20,000/mm3 and the absolute CD4 number was 100/mm3. We obtained a long-term correction of thrombocytopenia and, to a lesser extent, there was a stabilization of CD4 lymphocytes for 18 months. We observed a significant stimulation of natural killer (NK) function and an elevation in the serum level of tumor necrosis factor alpha, interferon gamma, and granulocyte-macrophage colony-stimulating factor. This suggests that in HIV-related ITP the removal of platelets is mediated by low-affinity Fc gamma receptors (CD16). The stimulation of NK function and elevation in CD4+ lymphocytes may be related to the production of cytokines by activated human NK cells through the interaction of their CD16-bearing receptor with the 3G8 monoclonal antibody. This observation warrants confirmation and further clinical trials.
 ...
PMID:Biologic response to anti-CD16 monoclonal antibody therapy in a human immunodeficiency virus-related immune thrombocytopenic purpura patient. 809 46

Neutrophils from patients with paroxysmal nocturnal hemoglobinuria (PNH) show a deficiency for the glycosylphosphatidylinositol- (GPI) linked Fc gamma receptor IIIb (Fc gamma RIIIb, CD16). The functional consequences of this defect are not clear. Here, we examined Fc gamma RIIIb-deficient neutrophils for their activation via Fc gamma receptors. Hydrogen peroxide (H2O2) production and change of intracellular free calcium [Ca2+]i were used as parameters for cell activation. Fc gamma RII and Fc gamma RIIIb stimulation was reached by cross-linking using fragments of monoclonal antibodies or incubation with monoclonal IgG cryoglobulin complexes. In parallel to the deficiency of Fc gamma RIIIb expression, H2O2 production and [Ca2+]i influx were decreased after cross-linking of Fc gamma RIIIb in PNH neutrophils compared with that for normal neutrophils. Stimulation via Fc gamma RII was not affected. Cryoglobulin complexes previously shown to activate normal neutrophils predominantly via Fc gamma RIIIb stimulated PNH neutrophils at a level not significantly weaker than controls. But this activation was mediated only via Fc gamma RII as shown by blocking studies. The results suggest that the loss of GPI-anchored Fc gamma RIIIb is functionally replaced by Fc gamma RII during the immune complex stimulation of PNH neutrophils. Therefore, the equipment of neutrophils with pleomorphic Fc gamma receptors prevents an immunodeficiency in PNH.
 ...
PMID:The loss of Fc gamma RIIIb in paroxysmal nocturnal hemoglobinuria is functionally replaced by Fc gamma RII. 820 83

The DiGeorge syndrome has been associated with various immune deficits. Embryologically, defects of the neural crest are associated with conotruncal and aortic arch abnormalities. The objective of this study was to determine if children with neural crest congenital heart defects can have subtle but significant immunodeficiencies. Complete blood counts with differential counts and a standard lymphocyte immunophenotyping panel of selected monoclonal antibodies were performed on peripheral blood from 20 children with neural crest cardiac disease and 34 normal newborns. The children with cardiac disease were grouped as survivors and nonsurvivors. The mean total white blood cell count was similar for all groups, but the percent lymphocytes was significantly less in the nonsurvivors than in the survivors and normal newborns (p < 0. 02). The lymphocyte subsets affected were CD2, CD3, and CD4. When the cardiac patients were compared to the normal newborns, again differences in lymphocyte subsets CD2, CD3, and CD4 were seen. When comparing nonsurvivors with survivors, the mean percentages of the CD2, CD3, and CD4 T lymphocyte markers, as well as the mean lymphocyte, B cell (CD20), and natural killer cell (CD16) percentages were all lower in the nonsurvivors. It was concluded that abnormalities in specific lymphocyte populations and their subsets may be predictors of infants at greatest risk for immunodeficiency complications. Therefore children with neural crest cardiac defects should have evaluations of lymphocyte subsets at birth and be treated as if potentially immunodeficient.
 ...
PMID:Abnormalities in lymphocyte populations in infants with neural crest cardiovascular defects. 866 26


1 2 Next >>