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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-CD3 monoclonal antibodies (mAb) have been shown to suppress T cell-mediated immune responses both in vitro and in vivo. However, in vitro studies with these antibodies have also demonstrated that they possess potent mitogenic properties, raising the possibility that they might be capable of potentiating immune responses in vivo. In this regard, we have recently shown that an anti-CD3 mAb can activate murine T cells in vivo. Furthermore, low doses of antibody induce interleukin 2 (IL-2) receptor expression and enhanced proliferation to allogeneic major histocompatibility complex (MHC) antigen without detectable modulation or blocking of the T cell receptor and without suppression of T cell-mediated immune responses. In light of these findings, we investigated the ability of low dose anti-CD3 to enhance an anti-tumor response directed against the malignant murine UV-induced skin tumor, 1591-Pro-4L. Low dose anti-CD3 administration resulted in enhanced in vitro anti-tumor activity and prevented tumor outgrowth in approximately two-thirds of animals treated at the time of tumor inoculation. Furthermore, these animals displayed lasting tumor-specific immunity. These results suggest that anti-CD3 mAb can be utilized for the enhancement of anti-tumor responses in vivo and may have general application in the treatment of immunodeficiency.
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PMID:In vivo administration of anti-CD3 monoclonal antibody can activate immune responses thus preventing malignant tumor growth. 297 18

The human immunodeficiency virus (HIV) and the closely related simian immunodeficiency virus (SIV) induce profound immune dysfunction in primate species. The present studies show that cell populations infected in vitro with SIV exhibit increases in major histocompatibility complex (MHC) class II antigen expression. Cell lines chronically infected with both the monkey and human viruses express substantially more MHC class II but not more lineage-restricted or activation antigens on their membranes than do uninfected cell lines. Furthermore, 2'-deoxy-5-iodouridine increased MHC class II antigen expression on SIV-infected cell lines in parallel with increased expression of viral antigens. MHC class II induction does not appear to be mediated through the production of a soluble factor, such as gamma interferon, by SIV-infected cells. Interestingly, studies of the kinetics of antigen expression by cell lines after SIV infection indicate that the induction of MHC class II structures is a late event. Immunoelectron microscopy revealed that MHC class II antigen is expressed not only on the surfaces of the SIV-infected cells but also on the envelope of virus particles derived from those cells. MHC antigen expression on virus-infected cells and the expression of those determinants by the virus may play a role in the pathogenesis of acquired immunodeficiency syndrome and the autoimmune abnormalities observed in HIV-infected individuals.
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PMID:Simian immunodeficiency virus induces expression of class II major histocompatibility complex structures on infected target cells in vitro. 303 70

The CD4 (T4) antigen was originally described as a phenotypic marker specific for helper T cells, and has recently been shown to be the receptor for the human immunodeficiency virus (HIV). Functional studies using monoclonal antibodies directed at CD4 and major histocompatibility complex (MHC) class II molecules led to the suggestion that CD4 binds to the MHC class II molecules expressed on stimulator cells, enhancing T-cell responsiveness by increasing the avidity of T cell-stimulator cell interaction and/or by transmitting a positive intracellular signal. But recent evidence that antibodies to CD4 inhibit T-cell responsiveness in the absence of any putative ligand for CD4 has been interpreted as suggesting that antibody-mediated inhibition may involve the transmission of a negative signal via the CD4 molecule instead. We have infected a murine T-cell hybridoma that produces interleukin 2 (IL-2) in response to human class II HLA-DR antigens with a retroviral vector containing CD4 cDNA. The resulting CD4-expressing hybridoma cell lines produce 6- to 20-fold more IL-2 in response to HLA-DR antigens than control cell lines. Furthermore, when antigen levels are suboptimal, the response of the cell lines is entirely CD4-dependent. The data presented here clearly demonstrate that CD4 can enhance T-cell responsiveness and may be crucial in the response to suboptimal levels of antigen.
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PMID:Expression and function of CD4 in a murine T-cell hybridoma. 303 88

It has been postulated that an acquired immunodeficiency syndrome develops in neonates as the result of a maternally induced graft-vs-host disease (GVHD) that develops when sufficient numbers of maternal lymphocytes are transferred to the fetus across the placental barrier. The present study was done to determine whether major histocompatibility complex (MHC) antigens or non-MHC minor histocompatibility antigens (MiHA) were involved. Female C57BL/6 mice were bred to males of eight selected strains such that maternal-fetal disparity existed at MHC antigens and/or minor histocompatibility antigens. Offspring were tested for immune function at 6-7 weeks of age using a Jerne plaque assay to measure the humoral response to that T dependent antigen sheep red blood cells (SRBC). None of the offspring developed clinical signs of GVHD, but 3 of 124 mice tested made no immune response to SRBC. Immunodeficiency was associated with maternal-fetal disparity only at a small number of MiHA and not at the MHC. We postulate that immunodeficiency in this model is mediated by a subclinical maternally induced GVHD to paternally derived MiHA of the fetus.
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PMID:Maternally induced graft-vs-host disease to minor antigens as a possible etiology of an acquired immunodeficiency syndrome in mice. 318 Jan 24

The T-cell surface glycoprotein CD4 is thought to function as a receptor for class II major histocompatibility complex molecules. Human CD4 is also the lymphoid cell receptor for human immunodeficiency virus, the causative agent of acquired immune deficiency syndrome. The observed infection of the central nervous system in acquired immune deficiency syndrome patients raises the possibility that CD4 is also present in nerve tissue and that a cell surface receptor for class II major histocompatibility complex antigens could play a role in central nervous system function. This possibility is reinforced by the detection of unique CD4-related transcripts in mouse and human brain tissue. In this study, the structure of the mouse brain CD4 transcript was determined. It is identical to the last two-thirds of the CD4 message and is capable of encoding a 217-residue protein that would consist of a truncated, 154-residue, cell surface region, together with the complete CD4 transmembrane and cytoplasmic regions. It would not include an amino-terminal hydrophobic leader peptide.
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PMID:Mouse brain CD4 transcripts encode only the COOH-terminal half of the protein. 326 Mar 31

The antigenic phenotype of human villous stromal macrophages (M phi s) from first and third trimester placentas was analyzed using a large number of monoclonal antibodies (MAbs) to monocyte (Mo)/M phi-associated cell membrane determinants. The purpose of this study was to investigate M phi phenotypic heterogeneity to create a database for the correlation of M phi phenotype with specific immunologic functions. The results showed that villous stromal mononuclear cells express many cell surface antigens found on Mo and M phi s and that they are morphologically diverse, ranging in appearance from classic Hofbauer cells to spindle-shaped cells with long cytoplasmic processes. Villous stromal M phi s were the numerically dominant cell type in this structure and exhibited some major phenotypic differences from M phi s in other tissues. Comparison of first- and third-trimester placentas revealed variation in antigen expression with increasing gestational age, in particular of class II major histocompatibility complex (MHC) determinants: HLA-DR and HLA-DP antigen density was low on first-trimester villous M phi s and much higher on third-trimester M phi s while HLA-DQ was undetectable in the first trimester but present on cells in third trimester placentas. The CD1 (T6) antigen, found on Langerhans (LH) cells and cortical thymocytes, was detected on villous M phi s by two thirds of the MAbs directed against different epitopes on this determinant. Furthermore, comparison with similar studies of lymphoid tissues showed that villous M phi s and dendritic cells share the expression of a number of other cell surface antigens. Finally, it was shown that M phi s in first- and third-trimester villi exhibit strong reactivity with MAbs (Leu 3a,b) to the CD4 antigen that serves as the receptor for the human immunodeficiency virus (HIV), suggesting that these cells may be a portal of entry or reservoir for this virus in the fetuses of pregnant, HIV+ women.
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PMID:The phenotype of human placental macrophages and its variation with gestational age. 326 59

Blood monocytes were analyzed in 28 patients with chronic lymphocytic leukemia without previous cytotoxic therapy and without recent infection. Using monoclonal antibodies and flow cytometry, monocytes identified by LeuM3 or My4 were low in percentage (2.3%), but absolute numbers were increased in many patients with values exceeding the normal range (120 to 510/microliter) in seven of 28 patients. Monocytosis was more prominent in patients with high leukemic counts, but there was no correlation to clinical stages. Monocytopenia was evident with less than 50 LeuM3+ cells/microliter in three patients. Two-color fluorescence was used for the analysis of cell surface expression of major histocompatibility complex (MHC) Class II molecules, complement receptors, and Fc receptors on the LeuM3+ monocytes. Compared to cells from control donors, there was an increase for MHC class II antigens, complement receptors, and Fc receptors on the monocytes in chronic lymphocytic leukemia, in terms of both the percentage of positive cells among the LeuM3+ monocytes and of fluorescence intensity. This increase was not restricted to patients with monocytosis nor were the molecules always upregulated concomitantly. The increase of antigen expression on LeuM3+ monocytes was more than 50% (1.5-fold) in seven of 22 patients for MHC Class II antigens, in seven of 16 patients for complement receptor and in six of 12 patients for Fc receptor. A similar decrease of antigen expression was observed only in one patient for MHC Class II and in one patient for complement receptor expression. Monocytosis and increased expression of monocyte cell surface antigens described for a large portion of patients might be causally involved in the immunodeficiency in chronic lymphocytic leukemia.
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PMID:Abnormal blood monocytes in chronic lymphocytic leukemia. 340 22

Phenotypic and functional analysis of B lymphocytes in two siblings with combined immunodeficiency associated with defective expression of class I and class II major histocompatibility complex (MHC) antigens on mononuclear cells is described. The results of the analysis of the membrane phenotype of the B cells performed at the age of 1 and 5 years, respectively, by the use of monoclonal antibodies against class I (HLA-A, -B, -C) and class II (HLA-DR, -DP, -DQ) MHC antigens showed a decreased expression of class I antigens and a complete lack of class II antigens. Class I antigen expression consistently remained of the same magnitude during follow-up. Class II antigen expression remarkably had been positive early in life on B cells and activated T cells, whereas monocytes were negative for class II from birth onward. B lymphocytes of both patients responded in vitro to polyclonal activation with Staphylococcus aureus Cowan I staphylococci (SAC) with the production of IgM-type immunoglobulins only. This neonatal type of response was in agreement with the membrane immunoglobulin phenotype of the B cells since a high sIgM/sIgD ratio characteristic of neonatal B cells was present. However, the expression of the FMC7 antigen on B cells of both patients was comparable to that on B cells of normal adults. We hypothesized that the lack of MHC antigen expression may impose a resting state on the lymphocytes in these patients due to ineffective cellular interactions. In this view the high sIgM/sIgD ratio reflects the activation state of the B cells rather than the maturational state of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenotypical and functional analysis of B lymphocytes of two siblings with combined immunodeficiency and defective expression of major histocompatibility complex (MHC) class II antigens on mononuclear cells. 349 42

The CD4 molecule, which is known to play an important role in the susceptibility of T lymphocytes to infection by the human immunodeficiency virus (HIV), is also expressed in small amounts on the surface of monocytes. Since monocytes can also be infected by the virus, we investigated peripheral blood monocytes of patients with the acquired immunodeficiency syndrome (AIDS), AIDS-related complex (ARC), and HIV seropositive and seronegative haemophiliacs without symptoms for the expression of the CD4 molecule and for other functionally important surface molecules such as CD11 (C3bi receptor), transferrin receptor, Fc receptor, and the three major histocompatibility complex (MHC) class II antigens HLA-DP, HLA-DR, and HLA-DQ. With immunofluorescence staining and flow cytometry no difference was found between patients and controls for the expression of the CD4 molecule and for the other antigens as assessed by the percentage of positive staining and the specific fluorescence intensity in a double marker analysis. The percentage of CD4+ monocytes was found to be 59.2 +/- 14.4% for 16 patients with AIDS and 52.9 +/- 12.8% for 12 healthy controls. Similar to our results on phenotype, we found no significant difference with respect to the production of tumour necrosis factor (TNF), in that monocytes of AIDS and ARC patients showed an increase in TNF secretion after stimulation with LPS comparable to controls.
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PMID:Monocyte phenotype and function in patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related disorders. 368 87

Development of cell-mediated immunity in young ruminants appears to be under the influence of the thymus. In sheep, prenatal removal of the thymus has little effect on postnatal growth of lambs. However, lambs are immunodeficient compared with normal controls, and they exhibit depressed delayed hypersensitive skin responses to antigens such as tuberculin purified protein derivative. Lymphopenia accompanying the immunodeficiency appears to be due to depletion of a particular population of T-cells (thymus derived) that have reduced response to mitogens and decreased numbers as the lamb matures. Young lambs are less responsive than adult sheep to vaccination with irradiated Trichostrongylus colubriformis larvae. The basis of this lowered responsiveness appears to be not only the immaturity of the cell-mediated immune response but also the segregation of the lambs into high and low responders. This immune responsiveness is possibly under the genetic control of the ovine major histocompatibility complex. It may be possible to select and breed sheep and cattle for responsiveness to vaccination against parasitic, viral, and bacterial diseases.
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PMID:Development of cell-mediated immunity in young ruminants. 388 81


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