Disease relevance of CD4-Positive T-Lymphocytes

• Predictive markers for the acquired immunodeficiency syndrome (AIDS) in hemophiliacs: persistence of p24 antigen and low T4 cell count [1].
• Other clinical and laboratory parameters such as p24 antigen, phytohemagglutinin mitogenic index, and absolute surface antigen T4+ cell counts did not accurately predict HIV fetal transmission [2].
• A tetra-, penta- or nonaribozyme under control of the SV40 late promoter, the beta-actin gene promoter or the HIV-1 LTR, respectively, were cotransfected with the infectious HIV-1 DNA clone pNL4-3 into permissive HeLa T4 cells [3].
• In this report, L and P proteins of the paramyxovirus simian virus 5 (SV5) were coexpressed in HeLa T4 cells from cDNA plasmids, and L-P complexes were examined [4].
• In the present study we have further investigated the fusion properties of F and HN proteins of parainfluenza virus type 1 (PI1), type 2 (PI2), and type 3 (PI3), Sendai virus (SN), and simian virus 5 (SV5) by expression of their glycoprotein genes in HeLa T4 cells using the vaccinia virus-T7 transient expression system [5].

High impact information on CD4-Positive T-Lymphocytes

• We report here that preincubation of T4+ lymphocytes with three individual monoclonal antibodies directed at the T4 glycoprotein blocked cell infection by LAV [6].
• Here, we show that transfectants expressing HLA-DR7 and either B7 or intercellular adhesion molecule 1 (ICAM-1) deliver independent costimulatory signals resulting in alloantigen-induced proliferation of CD4-positive T lymphocytes [7].
• Isolated T4+ cells ceased to respond to IL-2 well before T8+ cells, and before the disappearance of adequate levels of IL-2-R [8].
• Accordingly, T4+ cell autocrine IL-2 responsiveness is restricted by a mechanism that is independent of IL-2-R, and which ultimately results in cessation of both T4+ and T8+ cell IL-2-dependent clonal expansion [8].
• Since T4+ cells proliferate in an autocrine fashion to endogenous IL-2, whereas most T8+ cells respond in a paracrine fashion to IL-2 derived from T4+ cells, we thought it likely that a unique mechanism was operative to restrict T4+ cell IL-2-dependent autocrine proliferation [8].

Chemical compound and disease context of CD4-Positive T-Lymphocytes

• Processing protease for gp160 human immunodeficiency virus type I envelope glycoprotein precursor in human T4+ lymphocytes. Purification and characterization [9].
• Decrease in helper (T4+) lymphocytes following cimetidine treatment for duodenal ulcer [10].
• To investigate the possible role of calmodulin activity in HIV-1 replication, we investigated the anti-HIV activity of various CaM antagonists--trifluoperazine and naphthalenesulfonamide W13 or W7--in HeLa T4 cells, PBMCs, and various T lymphocytic cell lines [11].
• Inhibition of tryptase TL2 from human T4+ lymphocytes and inhibition of HIV-1 replication in H9 cells by recombinant aprotinin and bikunin homologues [12].
• The structure of this site has been constructed by the analysis of low-energy conformers of peptide T, an HIV reproduction inhibitor with amino acid sequence corresponding to the fragment Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr of protein gp120, ensuring the interaction of virus with T4 lymphocytes [13].

Biological context of CD4-Positive T-Lymphocytes

• In the group as a whole, the HLA haplotype A1 B8 DR3 was weakly associated with an increased risk of seroconversion on exposure to the virus while, in those who seroconverted, it was strongly associated with a rapid decline in T4 cells and development of HIV-related symptoms within four years of infection [14].
• Peptide specificity of alloreactive CD4 positive T lymphocytes directed against a major histocompatibility complex class I disparity [15].
• The nef protein expressed by vaccinia virus recombinants is phosphorylated by protein kinase C. We investigated the synthesis of the nef protein and its state of phosphorylation during HIV-1 infection of a T4 cell line (CEM cells) [16].
• Glutathione homeostasis is disturbed in CD4-positive lymphocytes of HIV-seropositive individuals [17].
• The observed decrease in T4/T8 ratio after cimetidine treatment is explained by a reduction in the number of T4+ cells and the appearance of a new subpopulation of T3-, T4-, T8-, B1-lymphocytes [10].

Anatomical context of CD4-Positive T-Lymphocytes

• Moreover, there was a significant correlation between a low percentage of T4+2H4+ cells and decreased suppressor-inducer function in autologous mixed lymphocyte reaction-activated T4+ cells from SLE patients [18].
• A murine monoclonal antibody (GA3) obtained by immunizing mice with cells of the human erythroleukemic cell line K562 is shown to define a 105 kilodalton (kd) membrane antigen on K562 cells that is restricted within the hematopoietic system to the erythroid lineage and to a minor population of CD3, CD4 positive T lymphocytes [19].
• To additionally characterize T cells responsible for CSF production, unfractionated T cells as well as T4+ and T4- cells were cloned by single cell micromanipulation [20].
• Anti-CD3 activated T4 cells did not inhibit initial B cell activation, but suppressed the capacity of the activated B cells to differentiate into ISC [21].
• These studies indicate that LCF interacts with T4+ lymphocytes and monocytes to induce migration and cellular activation [22].

Associations of CD4-Positive T-Lymphocytes with chemical compounds

• Isoprinosine and Imuthiol increased significantly both the percentage and the absolute number of T4+ cells when peripheral blood mononuclear cells were incubated for 4 days in RPMI supplemented with 10% fetal calf serum [23].
• Despite the ability to present nominal antigen, paraformaldehyde-fixed AC were unable to induce allogeneic T4 cell proliferation [24].
• These results suggest that LTB4 may regulate immune cell functions by inducing IFN-gamma production by T4+ cells [25].
• CD40 is a member of the tumor necrosis factor (TNF) family of receptors whose ligand (CD154) is mainly expressed on the membrane of activated CD4-positive lymphocytes [26].
• The response of highly enriched populations of human T8+ lymphocytes to the oxidative mitogenic enzymes neuraminidase (NA) and galactose oxidase (GO) was enhanced by NAGO-primed T4+ lymphocytes [27].

Gene context of CD4-Positive T-Lymphocytes

• The capacity of the monoclonal antibodies (Mab) 64.1 and OKT3 directed at CD3 molecules to induce T4 cell proliferation and interleukin 2 (IL 2) production was examined [28].
• Monoclonal antibodies against class II MHC (Ia) antigenic determinants blocked the AMLR between non-T cells and any of the above responder populations; in contrast, monoclonal anti-class I (HLA-A, B, C) antibodies inhibited the response of T8+ cells but not of isolated T4+ cells [29].
• To change the coreceptor usage of this vector from CCR5 to CXCR4, which is predominant on human CD4-positive lymphocytes, the putative V3-loop of SIVagm SU was replaced by that of the T cell tropic HIV-1 variant BH10 [30].
• The data indicate that in the absence of AC, a stimulatory matrix of immobilized 64.1 is sufficient for some T4 cells to be activated to become IL2 or IL4 responsive and for a smaller percentage to secrete IL2 [31].
• The results suggest that eosinophilia was caused by IL-5 and GM-CSF production by rhIL-2 stimulated CD4 positive lymphocytes [32].

Analytical, diagnostic and therapeutic context of CD4-Positive T-Lymphocytes

• In the control group, suppression mediated by T8+ cells exceeded that mediated by T4+ cells; such differences were not apparent in the MS group [33].
• Association was also sought between CIN and immunosuppression, as measured clinically by T4 cell number, beta-2-microglobulin and p24 antigen [34].
• Human peripheral T4 lymphocytes were obtained by venipuncture, propagated in RPMI 1640 medium and challenged with varied concentrations of aflatoxins, B1, B2, G1, and G2 [35].
• The qualitative PCR was more sensitive than the p24 antigen assay but the presence of the latter was predictive of progression of infection as determined clinically and by falling T4 cell counts and rising levels of beta 2M [36].

References