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 report a case of common variable immunodeficiency (CVI) that shows low levels of IgG and IgA, but a normal quantitative or qualitative level of IgM. T-cell functions were not disturbed. Increased numbers of surface IgM (sIgM) and sIgD, sIgM and sIgG, sIgM and sIgA double-bearing B cells were observed as compared with a control. No IgG and IgA induction upon stimulation with Staphylococcus aureus Cowan I (SAC) and recombinant interleukin-2 (rIL-2), or pokeweed mitogen (PWM) and rIL-4 or rIL-6 was observed, although there was proliferation. Although mu mRNA was expressed as much as in a healthy control, transcription of gamma mRNA and alpha mRNA was very low. Furthermore, no enhanced effects of gamma mRNA and alpha mRNA were recognized upon stimulation with rIL-4 and rIL-6. These results suggest that the patient's B cells might be defective at the switching process from mu, mu and delta, mu and gamma to gamma or mu and alpha to alpha.
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PMID:Common variable immunodeficiency with increased surface IgM-positive double-bearing B cells. 161 81

The phenotype and cytotoxic activity of lamina propria lymphocytes (LPL) from the colorectal mucosa have been investigated primarily to analyse the role of LPL in human immunodeficiency virus (HIV) infection. The results reported here show that LPL strictly required a proliferative stimulus [either interleukin-2 (IL-2) or phytohaemaglutinin (PHA) to develop strong in vitro cytotoxicity, since freshly isolated LPL do not exhert cytotoxicity against either natural killer (NK)-sensitive or NK-resistant target cells. The cytotoxicity of activated LPL against a large panel of myeloid tumours or colorectal carcinoma target cells shows the irrelevance of the tissue origin of target cells. Moreover, activated LPL lysed HIV-infected H9 cells more efficiently than peripheral blood lymphocytes (PBL), and were susceptible to HIV infection. In contrast, unstimulated LPL failed to be cytotoxic and susceptible to HIV. Thus, we strongly suggest that for the lymphocytes of the colorectal mucosa expression of cytotoxic activity and susceptibility to HIV-infection show two faces of the same coin, and therefore may be relevant in understanding the mechanisms and paths of transmission of HIV infection.
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PMID:Cytotoxic activity of intestinal lamina propria lymphocytes on human immunodeficiency virus (HIV)-infected cells. 162 89

The Authors report the isolation in Italy of Feline Immunodeficiency Virus (FIV) from a cat inoculated with whole blood from a naturally FIV infected cat. The virus was isolated in feline circulating leucocytes cultured in RPMI medium and stimulated with concanavalin-A and recombinant human interleukin-2. The infected cultures showed a characteristic cytopathic effect (ballooning degeneration, giant cell formation, cell death) and a specific fuorescence using FIV-positive cat serum and monoclonal antibodies against FIV. Furthermore, the culture supernatants contained magnesium-dependent reverse transcriptase activity.
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PMID:Isolation in Italy of feline immunodeficiency virus (FIV). 164 60

Production of interleukin-2 (IL-2) by human T-lymphocytes can be augmented by costimulation via CD28. It has been reported that signaling via CD28 acts by stabilization of lymphokine mRNAs (Lindsten, T., June, C. H., Ledbetter, J. A., Stella, G., and Thompson, C. B. (1989) Science 244, 339-343). Here we demonstrate that costimulation via CD28 also provides a signal which activates transcription of the IL-2 gene A CD28-responsive element (CD28RE) in the IL-2 enhancer at position -162 to -152 was identified. This so far unidentified element shows sequence similarity to the kB enhancer motif. In vitro binding studies have demonstrated that the via CD28-induced signal synergizes with either phorbol myristate acetate or anti-CD3 for the induction of a nuclear factor that binds CD28RE and the human immunodeficiency virus (HIV-1) NF-kB motif. The significance of the sequence similarity of CD28RE with the kB enhancer motif was demonstrated by cross-competition studies using unlabeled CD28RE, HIV-1 NF-kB binding site, and a mutated version of the NF-kB motif. In addition, we found that NF-kB-dependent reporter gene expression was induced by costimulation via CD28. These results indicate that besides an effect on lymphokine mRNA stabilization, stimulation via CD28 acts at the level of transcription via coinduction of an NF-kB-like activity.
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PMID:Activation of interleukin-2 gene transcription via the T-cell surface molecule CD28 is mediated through an NF-kB-like response element. 165 Mar 50

We present a patient with haemophilia A showing human immunodeficiency virus type 1 (HIV-1) infection and factor VIII inhibitor in whom a novel T-cell subpopulation, double-negative (CD4-CD8-) T cells bearing T-cell receptor (TCR)-alpha beta, proliferated polyclonally in the peripheral blood. An interleukin-2-dependent T-cell line with a CD4-CD8-TCR-alpha beta+ phenotype was established from the peripheral blood lymphocytes of the patient, and its biological functions were studied. It was found that the CD4-CD8-TCR-alpha beta+ T cells possessed both HLA-unrestricted cytotoxicity and helper function for immunoglobulin production by B cells. In addition, these T cells were found to produce interferon-gamma and interleukin-2 following activation via CD3-TCR complexes. These data demonstrating the multifunction of these newly defined CD4-CD8-TCR-alpha beta+ T cells thus suggest that these cells play an important role in protection against HIV infection. The mechanism of production of factor VIII inhibitor in the present case is also discussed focusing on the CD4-CD8-TCR-alpha beta+ T cells.
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PMID:Proliferation of double-negative (CD4-CD8-) T cells bearing T-cell receptor-alpha beta in a haemophiliac with human immunodeficiency virus type 1 infection and factor VIII inhibitor: functional properties of double-negative T-cell receptor-alpha beta+ T cells. 166 Nov 24

In ten chronic uremic patients on regular hemodialysis treatment in vitro experiments revealed that stimulation of opioid receptors with morphine did not significantly change the mitogen-induced proliferative response of peripheral blood lymphocytes and interleukin-2 (IL-2) receptor expression on PHA-stimulated lymphocytes, while it appreciably decreased surface transferrin (Trf) receptor expression on PHA-stimulated lymphocytes. However, metenkephalin inhibited mitogen-induced proliferation and surface Trf receptor expression on uremic lymphocytes without affecting IL-2 receptor expression on PHA-stimulated cells. In ten healthy subjects opioid receptor agonists did not significantly affect mitogen-induced proliferation of lymphocytes, except for the inhibitory effect of 10(-8) M morphine in relation to lymphocytes stimulated with an optimal pokeweed mitogen (PWM) concentration. At the same time, opioid receptor agonists depressed surface IL-2 and Trf receptor expression on PHA-stimulated normal lymphocytes. In most of our experiments naloxone itself, a non-selective competitive opioid receptor antagonist, decreased mitogen-induced lymphocyte proliferation and IL-2 and Trf receptor expression on PHA-stimulated lymphocytes. Moreover, most frequently naloxone did not reverse inhibitory effects of opioid receptor agonists on lymphocytes. The results seem to indicate that opioid receptor stimulation by high metenkephalin concentrations, which are observed in the uremic blood plasma, may share the responsibility for immunodeficiency in chronic uremic patients. Next, in the presence of opioid receptor agonists directions of changes in the mitogen-induced proliferative response may not follow the alterations of IL-2 and Trf receptor expression on both uremic and normal lymphocytes. Finally the results also suggest that naloxone may possibly exert effects which are independent of its action on opioid receptors on lymphocytes.
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PMID:Modification of some lymphocyte functions in vitro by opioid receptor agonists and antagonist in chronic uremic patients and healthy subjects. 166 19

Early studies with the Gross passage A leukemia virus demonstrated that retroviral infection suppresses cellular and humoral immune responses. In extensive studies of the feline leukemia (FeLV) virus, which can induce profound immunodeficiency disease, are generative anemia and lymphoid, myeloid and erythroid neoplasia, the immunosuppressive effects of this retrovirus could be attributed to the actions of the retroviral envelope protein p15E. We found that a highly conserved, synthetic 17 amino acid peptide synthesized by Cianciolo and co-workers that is homologous to the hydrophilic portion of the otherwise hydrophobic transmembrane envelope protein can suppress polyclonal activation of B-cells, impair production of gamma- and alpha-interferon, inhibit production of interleukin-2, inhibit expression of IL-2 receptors, and suppress responses of cytotoxic lymphocytes. In analyses with inactivated preparations of the human immunodeficiency virus, with Pahwa et al. we demonstrated that purified non-infectious retrovirus and also retroviral proteins, in particular gp120, appeared to produce some of the immunosuppressive properties of HIV, particularly suppression of B-cell activation in response to known B-cell stimulants irrespective of T-cell influence, suppression of T-helper cell functions essential to B-lymphocyte responsiveness, and impaired function of immunoglobulin-secreting cells. Other investigators have also reported strong immunosuppressive or immunostimulatory influences for components of the HIV retrovirus and also gp120 through yet poorly elucidated but certainly complex actions on both T- and B-lymphocyte-mediated immune functions.
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PMID:In vitro immunomodulation and in vivo immunotherapy of retrovirus-induced immunosuppression. 166 53

The safety of continuous i.v. interleukin-2 (IL-2) in conjunction with zidovudine (ZDV) was assessed in asymptomatic patients infected with human immunodeficiency virus. Clinical, immunologic, and viral parameters were monitored in a phase I/II trial with dose escalation and crossover arms. Daily doses of IL-2 from 1.5 to 12 x 10(6) IU/m2 were well tolerated and, in the presence of ZDV, did not induce increases in p24 antigenemia. Significant (p less than 0.05) but transient increases in CD4 cells were observed midway through infusion of IL-2 at all doses, and increases in natural and lymphokine-activated killer activity were seen at higher doses. Circulating hypodense eosinophils and soluble IL-2 receptors increased more than 10-fold. Of nine patients available for long-term follow up 13-25 months from baseline and 4-21 months after stopping IL-2, six still had improved CD4 counts (versus baseline), and the mean increase (135/mm3) for all nine patients was significant (p less than 0.05). Eight of these nine patients were negative for serum p24 at the start of therapy, and none had become p24 antigenemic at long-term follow-up.
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PMID:Safety and effects of interleukin-2 plus zidovudine in asymptomatic individuals infected with human immunodeficiency virus. 167 May 86

Helper T-cell function was evaluated in 34 children infected with human immunodeficiency virus type 1, by assessing interleukin-2 production after stimulation of peripheral blood mononuclear cells with recall antigens (influenza virus, tetanus toxoid), allogeneic HLA, and phytohemagglutinin. In addition, helper T-cell function was correlated retrospectively with the incidence of opportunistic and bacterial infections. Four patterns of helper T-cell function were observed: (1) 7 (21%) of the 34 children responded to all stimuli, (2) 7 (21%) of them responded to alloantigens and phytohemagglutinin but not to recall antigens, (3) 7 (21%) responded to phytohemagglutinin but not to recall antigens or alloantigens, and (4) 13 (37%) did not respond to any of these stimuli. There were no significant differences related to different routes of acquisition among patients. Patients with functional helper T-cell defects had a history of more opportunistic (p = 0.03) and bacterial (p less than 0.001) infections than did patients with intact helper T-cell function. Thus distinct patterns of helper T-cell dysfunction exist in children infected with human immunodeficiency virus type 1 and correlate with higher frequency of infections. Comparisons of in vitro helper T-cell responses to these stimuli may be useful for detecting early functional helper T-cell defects and for monitoring progression of disease.
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PMID:Helper T-cell responses in children infected with human immunodeficiency virus type 1. 167 68

Studies of lentivirus infection in ruminants, nonhuman primates, and humans suggest that virus infection of macrophages plays a central role in the disease process. To investigate whether human immunodeficiency virus type 1 (HIV-1) can infect chimpanzee macrophages, we recovered monocytes from peripheral blood mononuclear cells of HIV-1-negative animals and inoculated these and control human monocytes with a panel of four human-passaged monocytotropic virus strains and one chimpanzee-passaged isolate. HIV-1 infected human monocytes synthesized proviral DNA, viral mRNA, p24 antigen, and progeny virions. In contrast, except for the chimpanzee-passaged HIV-1 isolate, chimpanzee monocytes failed to support HIV-1 replication when cultured under both identical and a variety of other conditions. Proviral DNA was demonstrated only at background levels in these cell cultures by polymerase chain reaction for gag- and env-related sequences. Interestingly, the chimpanzee-passaged HIV-1 isolate did not replicate in human monocytes; viral p24 antigens and progeny virions were not detected. The same monocytotropic panel of HIV-1 strains replicated in both human and chimpanzee CD4+ T lymphoblasts treated with phytohemagglutinin and interleukin-2. The failure of HIV-1 to infect chimpanzee monocytes, which can be overcome by serial in vivo viral passage, occurs through a block early in the viral life cycle.
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PMID:The inability of human immunodeficiency virus to infect chimpanzee monocytes can be overcome by serial viral passage in vivo. 167 68


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