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Query: UMLS:C0021051 (
immunodeficiency
)
71,517
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A murine monoclonal antibody (MoAb) F101.01 reacting with the T cell receptor (TCR)-T3 complex is presented. Immunohistological studies showed that F101.01 specifically stains T-zone lymphocytes in lymph nodes, tonsils, and splenic tissue. Two-colour immunofluorescence and flow cytometry demonstrated co-expression of the antigen defined by F101.01 and the pan-T cell antigens defined by CD2, CD3,
CD5
, and CD7 antibodies. Cells stained with CD4 and CD8 antibodies were both included in the F101.01-positive population, whereas CD16-positive natural killer cells (NK), B cells (CD19 and CD20), and myeloid cells (CD13 and CD33) were excluded. The target antigen of F101.01 co-modulated with the CD3-defined antigen (T3) and the TCR recognized by the MoAb WT-31. CD3 antibody and WT-31 both blocked binding of F101.01. F101.01 precipitated the TCR-T3 complex from lysates of 125I-labelled peripheral blood mononuclear cells (PBMC) and HPB-ALL, when the lysate was prepared with a detergent (digitonin) that conserves the TCR-T3 complex. FACS analysis of T cells from a patient with a T cell
immunodeficiency
demonstrated that delta-TCS-1-CD3+CD4+ and delta-TCS-1-CD3+CD8+ cells were brightly F101.01+, whereas a large subpopulation of delta-TCS-1+CD3+CD4-CD8- cells were weakly F101.01+. We conclude that F101.01 recognizes a conformational epitope of the TCR-T3 complex and that it reacts with the alpha beta TCR-T3 and the gamma delta TCR-T3 complexes with different intensities.
...
PMID:Characterization and expression of the human T cell receptor-T3 complex by monoclonal antibody F101.01. 296 42
Activation of the enzyme protein kinase C (PKC) plays an important role in T cell activation. We investigated the phosphorylation of CD2, CD3, CD4,
CD5
, CD7, CD8, CD28 (Tp44), CD43 (sialophorin, gp115), and LFA-1 after incubation of human PBMC with the (PKC) activator PMA. These proteins were chosen for their role in transmembrane signal transduction (CD2, CD3,
CD5
, CD28, CD43), cell-cell interaction and adhesion (CD2, CD4, CD8, and LFA-1), or involvement in
immunodeficiency
states (CD43, CD7).
CD5
, CD7, CD43, and the alpha-chain of LFA-1 were found to be constitutively phosphorylated. PMA induced rapid hyperphosphorylation of
CD5
, CD7, and CD43, but not of the LFA-1 alpha-chain, and induced the phosphorylation of CD3, CD4, CD8 and of the LFA-1 beta-chain. PMA did not cause the phosphorylation of CD2 and CD28. PMA-induced phosphorylation was partially inhibited by the PKC inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride. Finally, the T cell activator Con A, which binds to the CD3/TCR complex was shown to induce a profile of protein phosphorylation similar to that observed with PMA. We conclude that PKC-mediated phosphorylation of T cell Ag may represent an important regulatory mechanism that governs the process of T cell activation.
...
PMID:Phosphorylation of T cell membrane proteins by activators of protein kinase C. 325 10
The authors present the results of immunophenotyping analysis of cells from 67 patients with the diagnosis of B-CLL from group of 393 adults examined by immunophenotyping because of a haematological malignity. Characteristic for B-CLL is the finding of surface molecules HLA DR, B lymphocytic superficial molecules and
CD5
. Aberrant membrane equipment of B-CLL cells is suggested by the rare absence of some pan B lymphocytic sign. Marked reduction of T lymphocyte ratios, their sub-populations and NK cells is associated with
immunodeficiency
manifestations which are common in patients with B-CLL.
...
PMID:[Immunophenotyping in chronic B-cell lymphatic leukemia]. 751 23
The surface membrane molecule
CD5
is expressed on mature T cells and on the B-1a subpopulation of B cells. These
CD5
positive B cells express an antibody repertoire with a relatively high frequency of self-reactivity. There is uncertainty about the origins of
CD5
B cells and the reasons for this are reviewed. Recent reports which relate to the lineage/selection debate are discussed. For instance, an increase in the frequency of
CD5
B cells is a feature of several genetically determined polysystem autoimmune syndromes. In the case of motheaten (me, mev) the pathogenesis of this increase in
CD5
B cells is not yet understood, even though the mutation has been mapped to the Hematopoietic cell protein-tyrosine phosphatase (Hcph) gene. Another mutation which affects B cell development, X-linked
immunodeficiency
(xid), encodes a point mutation in a B cell cytoplasmic tyrosine kinase. Expression of xid in otherwise normal mice causes a lack of
CD5
B cells and a shift in the antibody repertoire. Interestingly, expression of both xid and motheaten results in an amelioration of autoantibody production. Evidence is presented that in B cells regulation of expression of
CD5
can occur at the level of mRNA and that cross-linking of sIgM can induce the accumulation of
CD5
mRNA. The overall concept advanced is that cells expressing natural autoantibodies are triggered via sIgM ligation to become
CD5
B cells.
...
PMID:Activation of B-cells by sIgM cross-linking induces accumulation of CD5 mRNA. 753 70
We recently demonstrated that 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) prevented the infection of T cells by human
immunodeficiency
virus type-1 (Cardin et al., J. Biol. Chem. 266, 13355, 1991). In the present study we have used a panel of monoclonal antibodies (mabs) against a variety of human leukocyte antigens to characterize the interaction of DIDS by flow cytometry with various T cell surface molecules. DIDS blocked the specific immunoreactivity of mabs OKT4A and Leu 3A with CD4 on human leukemic T cells (JM) and human mononuclear lymphocytes with an IC50 approximately 30 microM. The membrane distal (D1) and proximal (D3 and D4) domains of CD4 remained blocked for up to 5 hr of culture and returned to control levels of expression after 24 hr, reflecting the rate of membrane turnover of the CD4-DIDS complex. The binding frequencies (% positive) for anti-CD2, -CD3, -
CD5
, -CD6, -CD7, -CD8, -CD11a, -CD14, -CD18, -CD19, -CD45, -T cell receptor, and -HLA-DR were not significantly affected. However, there was a partial reduction in the antigen density of CD2,
CD5
, CD8, and CD11b. The selective interaction of DIDS with CD4 suggests that antagonism of the virus receptor may account in part for the antiviral properties of the stilbene disulfonate.
...
PMID:Specific interaction of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid with human cellular CD4. 795 38
Normal differentiation of B lineage cells has been the subject of intensive investigation over the past three decades. Current models of this process in humans are melded from the results of studies in a variety of organisms, including humans, mice and birds. Several recent developments have significantly reshaped and refined these models. The technique of homologous recombination in embryonic stem cells has allowed the production of mice with selectively disrupted genes that are important for B cell development in mice. At the same time, functional studies of human B cell differentiation, together with analysis of naturally occurring mutations that disrupt this process, have progressed rapidly. This has provided insight into the pathogenesis of lymphoproliferative and
immunodeficiency
diseases as well as a clearer view of normal developmental events. In this chapter we have reviewed human B cell differentiation with particular emphasis on newly emerging concepts. We also discussed
CD5
, a pan-T cell antigen that is expressed in low levels on a subpopulation of B cells implicated in the pathogenesis of chronic lymphocytic leukaemia (CLL). Finally, we discussed the issue of restricted variable region gene usage during B cell ontogeny and in CLL.
...
PMID:Normal B lymphocyte differentiation. 803 90
A 31-year-old renal transplant recipient developed an unusual T-cell lymphoproliferative disorder 3 years after transplantation. The neoplasm involved the spleen, without concomitant hepatomegaly, lymphadenopathy, or obvious bone marrow involvement. Peripheral blood involvement developed after splenectomy. Immunophenotypically, the neoplastic cells expressed CD2, CD3, CD7, CD16, CD45, CD56, and the gamma/delta T-cell receptor on the surface membrane. The neoplastic cells were negative for surface membrane CD4,
CD5
, and CD8. Serologic and/or DNA analyses for viruses, including Epstein-Barr virus, human T-cell lymphotropic virus-1, human
immunodeficiency
virus, and human herpesvirus-6, were negative. Cytogenetic findings included a translocation breakpoint at chromosome 7p15, consistent with involvement of the T-cell receptor gamma-chain locus. Although gamma/delta T-cell lymphomas have been reported to have a predilection for hepatosplenic localization, this is the first well-documented case to be described in the setting of posttransplantation immunosuppression.
...
PMID:Gamma/delta T-cell posttransplantation lymphoproliferative disorder primarily in the spleen. 808 54
Rabbits can be infected with human retroviruses such as human T-cell leukemia virus-1 (HTLV-1) and human
immunodeficiency
virus (HIV), and provide useful animal models to study retroviral diseases such as adult T-cell leukemia and HIV. Previously we have succeeded in generating monoclonal antibodies (mAbs) against rabbit CD4,
CD5
and CD11a antigens. To make this animal species more amenable to cellular and molecular studies, we have attempted to extend the panel of mAbs against rabbit CD antigens. Here we report on the generation of three neutralizing mAbs against interleukin-2 receptor alpha chain (IL-2R alpha) (CD25), Kei-alpha 1 (IgG2b), Kei-alpha 2 (IgG2a) and Kei-alpha 3 (IgG1). They specifically recognize the rabbit Mr 55,000 IL-2 binding protein, IL-2R alpha, and completely inhibit both high- and low-affinity IL-2 binding to F648b cells that express IL-2R alpha as well as IL-2R beta. The use of mAb Kei-alpha 1 confirmed that the rabbit IL-2R alpha is not only a low-affinity IL-2R on its own but also an essential component of high-affinity IL-2R as found in other animal species, and that rabbit activated T cells including HTLV-1-transformed cell lines express high levels of the IL-2R alpha. Together with mAbs against various rabbit CD antigens that we reported previously, these neutralizing mAbs to IL-2R alpha will be valuable for studies of human retrovirus infections, such as those induced by HTLV-1 or HIV, in rabbits.
...
PMID:Generation of monoclonal antibodies to the rabbit interleukin-2 receptor alpha chain (CD25) and its distribution in HTLV-1-transformed rabbit T cells. 837 Jun 51
We tested the susceptibility of human purified, normal B lymphocytes to human
immunodeficiency
virus type 1 (HIV-1) infection, in the presence or absence of complement-sufficient serum and of virus-specific antibodies. Virus replication was detected when cells were infected in the presence of both complement and anti-HIV antibodies (C'-ADE conditions), by day 2 postinfection. Similar results were obtained when B lymphocytes were purified either from peripheral blood (three healthy donors) or from tonsils (four individuals with chronic tonsillitis). HIV infection was shown by polymerase chain reaction (PCR) detection of proviral sequences (gag and pol genes), by p24 antigen synthesis, and by cocultivation assay with MT2 cells. The higher p24 production was obtained when B cells were preactivated for 2 days by phorbol 12-myristate 13-acetate (PMA) before infection and then cultured in the presence of low-molecular weight B-cell growth factor (LMW-BCGF). Expression of virus envelope glycoprotein (gp) 120 could also be detected on a subpopulation of B cells (CD19+, CD22+) by flow cytometry. Blocking experiments with monoclonal antibodies (MoAbs) against CD4, CD21 (complement receptor 2 [CR2]), CD35 (CR1), CD19, and
CD5
surface molecules indicated that infection of B cells involves CD4, CD21, and CD35 antigens. Indeed, blocking of CD4 receptor inhibited 10% of p24 production, and blocking of both CD21 and CD35 led to extinction of p24 signal. CR-dependent pathway is thus a major route for C'-ADE of HIV infection in normal B cells. Our results emphasize the importance of studying interactions between HIV and the complement system for better understanding infection mechanisms and the major dysfunctions of B cells in HIV-infected individuals.
...
PMID:Complement and virus-specific antibody-dependent infection of normal B lymphocytes by human immunodeficiency virus type 1. 846 67
Chronic alcoholics are frequently immunodeficient, have polyclonal hypergammaglobulinaemia, and often have autoantibodies. Recent work in other diseases has shown that functional distinctions of possible relevance to autoimmunity and
immunodeficiency
can be found among the B cell subsets defined by differential expression of the surface markers
CD5
and CD45RA. Therefore, we have evaluated the
CD5
, CD45RA B cell subsets of both chronic alcoholics without evidence of active liver disease (AWLD), and alcoholics admitted for acute alcoholic liver disease (ALD). Mean B cell numbers were normal in AWLD, but significantly reduced in ALD. Analysis of B cells by three-colour flow cytometry in 20 patients and 29 controls revealed a sharp decrease in the percentage of alcoholics' B cells which were CD5+, 37.6% versus 16.3%, P < 0.000 01; absolute CD5+ B cell numbers were similarly reduced (58.9 cells/microliters versus 20.9; P = 0.0012). In addition to the loss of CD5+ B cells, there was a reduction in the percentage of B cells which are
CD5
- CD45RAhi, leaving many patients with a B cell profile which was predominantly CD19+
CD5
- CD45RAlo. This subset appears phenotypically similar to the IgM-producing
CD5
- CD45RAlo subset described by others, and may be enriched for autoantibody-producing cells. One outlier patient was an ALD with 61% of B cells which were CD5+, which also is a profile consistent with increased autoantibody production.
...
PMID:Loss of the CD5+ and CD45RAhi B cell subsets in alcoholics. 856 16
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