D J Carlo

William Penn University, Filadelfia, Pennsylvania, United States

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Publications (102)428.02 Total impact

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    ABSTRACT: Propofol hemisuccinate is a prodrug water soluble form of the lipophilic, phenolic compound propofol (2,6-di-isopropylphenol), that is the active ingredient in the widely used anesthetic agent Diprovan. Propofol binds to GABA(A) receptors but also has a phenolic structure that confers antioxidant properties to the molecule. The effects of propofol hemisuccinate in rat experimental autoimmune encephalomyelitis (EAE) were studied using different doses and time regimes. Propofol hemisuccinate, 100 mg/kg given three times a day from day 7 or day 12 until day 16 after disease initiation, significantly reduced maximal EAE score. Histology studies supported the clinical findings demonstrating reduction in the inflammatory response in the lumbar spinal cord in animals treated with propofol hemisuccinate. Decreased levels of nitrotyrosine and unchanged levels of induced nitric oxide synthase suggest propofol hemisuccinate crossed the blood brain barrier and exerted its effects by lowering reactive oxygen species levels. The results suggest that propofol hemisuccinate may provide an alternative mode of treatment for acute exacerbations of multiple sclerosis.
    Autoimmunity 06/2007; 40(3):180-6. DOI:10.1080/08916930701204467 · 2.71 Impact Factor
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    ABSTRACT: Restricted T-cell receptor Vβ gene use in animal models of autoimmune disease has led to the development of strategies to treat autoimmune disease by targeting the T-cell receptors of the pathogenic T-cells. Restricted T-cell receptor gene use has been noted in human autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. We report here the finding of restricted T-cell receptor gene use in psoriasis vulgaris, as well. Our results show an elevated skin (over PBL) expression of Vβ3 and/or Vβ13.1 messages in the CD8+ T-cells in a majority of patients studied. CDR3 sequence analysis on these two Vβs from the skin demonstrated monoclonality or marked oligoclonality. A second biopsy performed 3.5 to 8 months later in four patients, at the same or different lesions, again revealed an elevated Vβ3 and/or Vβ13.1 expression and clonality. Moreover, in three of the four patients, the same TcR Vβ CDR3 rearrangement was found in both biopsies, although there was no Vβ CDR3 homology noted between patients. In two patients in which Vβ3 and/or Vβ13.1 was not elevated in the CD8+ T-cell population, an increase in Vβ17 gene use and clonality was found. The persistence of Vβ3- and/or Vβ13.1-bearing CD8+ T-cells in lesions that did not undergo resolution suggests their role as effector cells rather than as regulatory cells. The effector function of these CD8+ T-cells is further supported by the clonality of TcR Vβ sequence data, which indicates they are recruited and expanded in situ. The Vβs identified in this study are candidate targets for selective immunotherapeutic intervention in psoriasis.
    Annals of the New York Academy of Sciences 12/2006; 756(1):370 - 381. DOI:10.1111/j.1749-6632.1995.tb44541.x · 4.38 Impact Factor
  • Annals of the New York Academy of Sciences 12/2006; 756(1):211 - 214. DOI:10.1111/j.1749-6632.1995.tb44514.x · 4.38 Impact Factor
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    W Soo Hoo · E R Jensen · A Saadat · D Nieto · R B Moss · D J Carlo · T Moll
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    ABSTRACT: Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of this situation is underscored by the emergence of new potentially human pathogenic influenza strains, avian H5N1 being the most recent example. We present evidence that antibodies against T cell immunoglobulin mucin-1 (TIM-1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross-strain immune reactivity. To determine potential immunostimulatory properties of anti-TIM-1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM-1-specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen-specific lymphocyte proliferation and cytokine production. Results show that TIM-1 antibodies enhance antigen-specific cellular proliferation (P < 0.05) and interferon (IFN)-gamma production (P < 0.01). Using blocking anti-CD4 and CD8 antibodies, it was observed that antigen-specific cellular proliferation is CD4-dependent and that the majority of proliferating cells are CD4+. Finally, vaccination with inactivated influenza virus with TIM-1 antibody results in the significant (P < 0.001) induction of proliferation and IFN-gamma production upon stimulation with one of three serologically distinct strains. TIM-1 antibodies demonstrate an adjuvant effect promoting antigen-specific cellular proliferation and IFN-gamma production, which are important for the promotion of cell-mediated immunity. These results are the first to suggest that TIM-1 antibody may serve as a potent adjuvant in the development of new influenza virus vaccines.
    Clinical & Experimental Immunology 08/2006; 145(1):123-9. DOI:10.1111/j.1365-2249.2006.03107.x · 3.04 Impact Factor
  • Clinical & Experimental Immunology 07/2006; 145(1):123-129. DOI:10.1046/j.1365-2249.1998.00503.x-i1 · 3.04 Impact Factor
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    ABSTRACT: The T-cell Ig and mucin domain-containing (TIM) gene locus has been linked to differences in T(H)2 responsiveness and asthma susceptibility in mice. The homologous locus in human subjects harbors the gene for TIM-1, which encodes a receptor for hepatitis A virus and has been linked with decreased susceptibility to atopic disease in hepatitis A virus-seropositive individuals. We investigated the effects of administering antibodies against TIM-1 in a mouse model of allergic asthma to determine whether the treatment could downregulate T(H)2 cytokines and reduce pulmonary inflammation. BALB/c mice were sensitized and challenged with ovalbumin to induce airway inflammation. Before the ovalbumin challenge, mice were treated with anti-TIM-1 mAb or a control antibody. Administration of anti-TIM-1 antibody to mice after ovalbumin sensitization and before ovalbumin challenge results in a significant decrease in inflammatory cells in bronchoalveolar lavage fluid compared with administration of a control antibody. The decrease is accompanied by significantly lower antigen-specific production of the T(H)2 cytokines IL-10 and IL-13 by cells from the draining lymph nodes. The T(H)1 cytokine IFN-gamma appears to be unaffected. Analysis of the lungs shows that goblet cell hyperplasia and mucus production and the expression of IL-10 are markedly decreased in anti-TIM-1-treated mice. The results indicate that anti-TIM-1 might offer a novel approach to treating asthma.
    Journal of Allergy and Clinical Immunology 01/2006; 116(6):1343-9. DOI:10.1016/j.jaci.2005.08.031 · 11.48 Impact Factor
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    R. B. Moss · E. Janssen · D. Nieto · J. A. Encinas · D. J. Carlo
    Journal of Allergy and Clinical Immunology 04/2005; 115(4):891-891. DOI:10.1016/j.jaci.2005.01.046 · 11.48 Impact Factor
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    ABSTRACT: Inflammation is initiated as a protective response by the host, but can often result in systemic pathology. Among cells of the immune system, T lymphocytes play a major role in the inflammatory response. T cell inflammation is characterised histologically by an infiltration of mononuclear cells. Key regulators of this response are a subset of T lymphocytes called T helper (Th) cells. These cells secrete soluble mediators called cytokines, which orchestrate the immune response. The appropriate regulation of Th cell immunity is critical in the control and prevention of diverse disease states. This review will focus on the role of Th cells in the inflammatory process involved in allergic disease, diabetes, infectious disease, rheumatoid arthritis, heart disease, multiple sclerosis and cancer. In the area of autoimmunity, in particular, a basic understanding of Th cells and cytokines has contributed to the development of clinically efficacious biological agents. This review also examines current and novel treatment strategies under investigation at present that regulate Th cell immunity, which may result in better treatments for immune-mediated diseases.
    Expert opinion on biological therapy 01/2005; 4(12):1887-96. DOI:10.1517/14712598.4.12.1887 · 3.74 Impact Factor
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    ABSTRACT: Differential gene expression in the rat after injury of dorsal root ganglion neurons in vivo, and simulation injury of Schwann cells and oligodendrocytes in vitro was analyzed using high-density cDNA microarrays. The analyses were carried out to study the genetic basis of peripheral nerve regeneration, and to compare gene regulation in glia of the central (oligodendrocyte) and peripheral (Schwann cell) nervous systems. The genes showing significant differential regulation in the three study groups represented all aspects of cellular metabolism. However, two unexpected observations were made. Firstly, a number of identical genes were differentially regulated in activated Schwann cells, activated oligodendrocytes and regenerating DRG neurons. Specifically, a group of 113 out of 210 genes that were down-regulated in Schwann cells upon lipopolysaccharide (LPS) treatment, were identical to genes up-regulated in the injured, regenerating DRG. Furthermore, a group of 53 out of 71 genes that were down-regulated in interferon gamma (IFN-gamma)/LPS-activated oligodendrocytes, were identical to genes up-regulated in the DRG neurons. Finally, 22 genes were common to these three groups, i.e., down-regulated in activated oligodendrocytes, down-regulated in activated Schwann cells, and up-regulated in regenerating DRG neurons. Secondly, a group of 16 cell-cycle and proliferation-related genes were up-regulated in the DRG following sciatic nerve crush, despite the absence of cells undergoing mitosis in the DRG, or any significant presence of apoptosis-related gene expression. Therefore, it appears that in these three cell types, large sets of genes are reciprocally regulated upon injury and/or activation. This suggests that the activation of the injury-related gene expression program in cell derivatives of the neuroectoderm involves, in part, highly conserved genetic elements.
    Journal of Cellular Biochemistry 04/2003; 88(5):970-85. DOI:10.1002/jcb.10392 · 3.26 Impact Factor
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    ABSTRACT: The immunologic correlates associated with control of viremia in HIV disease are poorly understood. We hypothesized that structured antiviral drug treatment interruptions could be utilized to better understand the relationship between HIV-specific immunity and viral replication. We thus examined the effects of two 8 weeks antiviral structured treatment interruptions (STIs) in a cohort of HIV-1 chronically infected individuals on highly active antiretroviral treatment (HAART) with (n = 13) and without (n = 12) therapeutic HIV immunizations. In this study, we observed that p24 gag antigen (np24) stimulated MIP-1beta levels and T helper immune responses prior to antiviral drug discontinuation were associated with control of viremia. Stronger and earlier production of gag peptide stimulated gamma interferon was observed in the immunized group during the structured antiviral drug interruptions. These results support the concept that HIV-specific immune responses are associated with control of viremia. Further study of immune-based therapies that enhance HIV-specific immunity is warranted.
    Vaccine 04/2003; 21(11-12):1066-71. DOI:10.1016/S0264-410X(02)00610-2 · 3.62 Impact Factor
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    ABSTRACT: After a single IV injection of the water-soluble propofol prodrug propofol phosphate (PP) in mice, rats, rabbits, and pigs, propofol was produced rapidly (1-15 min), inducing dose-dependent sedative effects. In mice, the hypnotic dose (HD(50)), lethal dose (LD(50)), and safety index (defined as a ratio: LD(50)/HD(50)) were 165.4 mg/kg, 600.6 mg/kg, and 3.6, respectively. Propofol was produced with half-lives of 5.3 +/- 0.6 min in rats, 2.1 +/- 0.6 min in rabbits, and 4.4 +/- 2.4 min in pigs. The maximal concentration was dose and species dependent. The elimination half-life was 24 +/- 12 min in rats, 21 +/- 16 min in rabbits, and 225 +/- 56 min in pigs. Propofol generated from PP produced pharmacological effects similar to those described in the literature. We found a correlation between PP dose and duration of sedation with propofol concentrations larger than 1.0 microg/mL, which produced somnolence and sedation in rats and pigs. Adequate sedation and, at large enough doses, anesthetic-level sedation were produced after the administration of PP. Overall, PP, the water-soluble prodrug of propofol, seems to be a viable development candidate for sedative and anesthetic applications. IMPLICATIONS: Propofol phosphate, a water-soluble prodrug of the widely used IV anesthetic propofol, was developed and evaluated in mice, rats, rabbits, and pigs after IV injection. The results of the study clearly demonstrate the feasibility of the prodrug approach to achieve sedative and anesthetic levels of propofol in laboratory animals; this warrants further evaluation in humans.
    Anesthesia & Analgesia 12/2002; 95(5):1285-92, table of contents. DOI:10.1097/00000539-200211000-00034 · 3.47 Impact Factor
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    ABSTRACT: Cancer vaccines composed of tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor (GM-CSF) are currently being clinically evaluated. To enhance the immunogenicity of GM-CSF-secreting tumor cell vaccines, a novel approach expressing GM-CSF as a membrane-bound form (mbGM-CSF) on the tumor cell surface was investigated. The intent was to enhance antigen presentation by increasing interactions between the tumor cell lines in the vaccine and GM-CSF receptor positive antigen presenting cells (APC), notably the patient's Langerhans cells residing within the intradermal injection site. B16.F10 cells engineered to express either membrane-bound or secreted GM-CSF were compared in the B16.F10 mouse melanoma model. We observed that mbGM-CSF on the tumor cell surface retarded growth and induced protective immunity to subsequent wild-type tumor challenge more effectively than tumor cells secreting GM-CSF. Vaccination with irradiated mbGM-CSF B16.F10 also provided strong protection from wild-type tumor challenge, improved therapeutic effects against established tumors, and retarded lung metastases. These results demonstrate that mbGM-CSF B16.F10 cells can induce strong systemic immunity that protects against and therapeutically treats B16.F10 melanoma more effectively than analogous vaccines containing only secreted GM-CSF. These data warrant further development and clinical testing of mbGM-CSF tumor cell vaccines.
    Gene Therapy 11/2002; 9(19):1302-11. DOI:10.1038/sj.gt.3301803 · 3.10 Impact Factor
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    ABSTRACT: Acquired or inherent drug resistance is the major problem in achieving successful cancer treatment. However, the mechanism(s) of pleiotropic drug resistance remains obscure. We have identified and characterized a cellular metabolic strategy that differentiates drug-resistant cells from drug-sensitive cells. This strategy may serve to protect drug-resistant cells from damage caused by chemotherapeutic agents and radiation. We show that drug-resistant cells have low mitochondrial membrane potential, use nonglucose carbon sources (fatty acids) for mitochondrial oxygen consumption when glucose becomes limited, and are protected from exogenous stress such as radiation. In addition, drug-resistant cells express high levels of mitochondrial uncoupling protein 2 (UCP2). The discovery of this metabolic strategy potentially facilitates the design of novel therapeutic approaches to drug resistance.
    The FASEB Journal 11/2002; 16(12):1550-7. DOI:10.1096/fj.02-0541com · 5.04 Impact Factor
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    ABSTRACT: We examined immunization with an inactivated, gp120-depleted human immunodeficiency virus (HIV) antigen in incomplete Freund's adjuvant (IFA), also containing a sequence of immunostimulatory (ISS) DNA, during the last trimester of pregnancy and neonatally in a rat model. Pregnant rats were immunized in the third trimester and their litters were immunized during the newborn period. In addition, litters of rats from non-immunized mothers were immunized during the neonatal period. As another control, pregnant rats were immunized and their litters analysed. Supernants from peripheral blood mononuclear cells (PBMCs) were assayed from newborns at 4 weeks of age for HIV-specific interferon-gamma (IFN-gamma), HIV-specific regulated on activation, normal, T-cell expressed, and secreted (RANTES), and serum for p24 antigen-specific immunoglobulin G (IgG) production. In the animals whose pregnant mothers were immunized and were also immunized during the neonatal period, we observed HIV-specific IFN-gamma production and HIV-specific RANTES production, but weak p24 IgG antibody production. Animals immunized only during the neonatal period developed the highest levels of HIV-specific IFN-gamma production, but somewhat lower levels of HIV-specific RANTES and p24 IgG antibody production. The group of animals whose mothers had received immunizations during the last trimester of pregnancy, but were not immunized during the neonatal period, developed the strongest p24 IgG antibody levels, but little or undetectable HIV-specific IFN-gamma or RANTES production. Neonatal immunization resulted primarily in cell-mediated immune responses, while animals born to mothers who were immunized during the last trimester had primarily an antibody-mediated immune response. Immunization of pregnant animals followed by neonatal immunization resulted in a mixed cell-mediated/antibody type profile in the neonatal animal. Future studies should provide insights into neonatal immunity and potential vaccine approaches to prevent neonatal infection and perinatal transmission.
    Immunology 09/2002; 106(4):549-53. DOI:10.1046/j.1365-2567.2002.01464.x · 3.80 Impact Factor
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    ABSTRACT: We report the immunological characterization of three colon carcinoma cell lines, COLO 205, SW620 and SW403, which we selected to combine with cytokine-secreting fibroblasts for the development of an allogeneic tumour cell vaccine. The cell lines expressed HLA-A2 as well as shared tumour-associated antigens (TAAs) representative of colon carcinomas: CEA, Ep-CAM, MUC1, HER2/neu and MAGE antigens. They did not secrete high levels of the immunosuppressive factors TGF-beta, IL-10 or prostaglandins. The lines presented TAAs in a manner recognized by immune effector cells, which was demonstrated by the lysis of SW620 by HLA-A2-restricted anti-p53 cytotoxic T lymphocytes (CTL). COLO 205 and SW620 were genetically modified to express the co-stimulatory molecule CD80 (B7.1), which increased the ability of the cells to stimulate CTL in vitro. CTL clones derived from HLA-A2+ peripheral blood mononuclear cells stimulated with the CD80-expressing lines lysed the stimulator cell and an HLA-A2+ colon cancer cell line, but did not lyse an isogeneic fibroblast line or an HLA-A2- colon cancer cell line. CTL clones derived from colon carcinoma patients immunized with an allogeneic vaccine containing these lines demonstrated killing of autologous tumour cells, the vaccine cell lines and other HLA-A2+ colon cancer cell lines, but not fibroblasts isogeneic to certain of the target cell lines. Our studies demonstrate that these colon carcinoma cell lines express shared TAAs that can induce CTLs which recognize and lyse other colon carcinoma cells, and support the continued clinical evaluation of the CD80 gene modified allogeneic colon cell/cytokine-secreting fibroblast carcinoma vaccine.
    Clinical & Experimental Immunology 08/2002; 129(1):99-106. DOI:10.1046/j.1365-2249.2002.01863.x · 3.04 Impact Factor
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    ABSTRACT: We treated a cohort of 38 HIV-infected individuals with a therapeutic vaccine (REMUNE, HIV-1 Immunogen) in an open label study. We then determined whether baseline parameters, such as CD4 cell count, viral load and IgG levels, were predictive of the magnitude of the HIV-specific lymphocyte proliferative responses (LPRs). We demonstrate herein that there is a significant enhancement from baseline for both HIV and p24 antigen-stimulated LPRs after immunization. Using a responder definition of a stimulation index of >5 on at least two post-immunization time-points, 29/38 (76%) responded to HIV-1 antigen while 27/38 (71%) responded to native p24 antigen. Viral load and total IgG were negatively correlated, while CD4 cell counts were positively associated with the magnitude of the HIV antigen LPR. In a multivariable analysis, baseline CD4 was the best predictor of HIV antigen LPR post-immunization.
    Clinical & Experimental Immunology 05/2002; 128(2):359-64. DOI:10.1046/j.1365-2249.2002.01835.x · 3.04 Impact Factor
  • Methods in molecular medicine 02/2002; 69:1-13.
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    ABSTRACT: The purpose of this 2-year follow-up study was to investigate the long-term effect of Remune as monotherapy for HIV-1 infection. Participants previously enrolled in the phase II double-blind, randomized, adjuvant-controlled study of the HIV-1 Immunogen (Remune) were followed for 2 years. Open-label immunization with Remune monotherapy was given to each participant every 12 weeks. Remune, a gp 120-depleted HIV-1 that was inactivated in beta-propiolactone and irradiation, was emulsified with mineral oil (incomplete Freund's adjuvant). In Study 2101B, the effect of four doses of Remune given every 12 weeks over 40 weeks was compared to placebo in 297 asymptomatic type E HIV-infected patients [Churdboonchart et al., 2000]. A group of 17 volunteers were separated into a subset study and another 57 were excluded from analysis due to discontinuation or addition of other treatments. This 2-year follow-up study continued with open-label dosing of HIV-1 Immunogen every 12 weeks for the remaining 223 patients. Changes in CD4+ cells, CD8+ cells, and body weight were monitored at each patient visit. Overall, immunizations were safe; common adverse events were tolerable injection site reactions. CD4+ T-cell counts remained stable over the 132-week observation period for this cohort with a slight increase of 36.01 cells/microL. CD8+ T-cell counts showed an increase from baseline during the follow-up period (415.21 cells/microL). Furthermore, we also observed an increase in body weight from baseline (1.08 kg) at week 132. In addition, baseline CD4 count appeared to predict CD4 count at week 132 (slope = 0.31, p <.0001). These results suggest that long-term treatment of HIV-1 infection with Remune monotherapy is safe and results in a stabilization of CD4+ counts. Furthermore, it is likely that HIV-1 therapeutic immunization may show its greatest clinical benefit in participants with higher CD4+ cell counts. Such an approach may have important ramifications in developing countries where access to antiviral drugs is limited and also in early chronic HIV-1 infection when CD4+ cells are still over 300 cells/microL in order to limit the cost and toxicity.
    HIV Clinical Trials 09/2001; 2(5):391-8. DOI:10.1310/Q5XX-A5CH-XTB9-FN33 · 2.63 Impact Factor
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    ABSTRACT: Inflammatory Th1 cells reacting to tissue/myelin derived antigens likely contribute to the pathogenesis of diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), and psoriasis. One regulatory mechanism that may be useful for treating autoimmune diseases involves an innate second set of Th2 cells specific for portions of the T cell receptor of clonally expanded pathogenic Th1 cells. These Th2 cells are programmed to respond to internally modified V region peptides from the T cell receptor (TCR) that are expressed on the Th1 cell surface in association with major histocompatibility molecules. Once the regulatory Th2 cells are specifically activated, they may inhibit inflammatory Th1 cells through a non-specific bystander mechanism. A variety of strategies have been used by us to identify candidate disease-associated TCR V genes present on pathogenic Th1 cells, including BV5S2, BV6S5, and BV13SI in MS, BV3, BV14, and BV17 in RA, and BV3 and BV13S1 in psoriasis. TCR peptides corresponding to the mid region of these BV genes were found to be consistently immunogenic in vivo when administered either i.d. in saline or i.m. in incomplete Freund's adjuvant (IFA). In MS patients, repeated injection of low doses of peptides (100-300 microg) significantly boosted the number of TCR-reactive Th2 cells. These activated cells secreted cytokines, including IL-10, that are known to inhibit inflammatory Th1 cells. Cytokine release could also be induced in TCR-reactive Th2 cells by direct cell-cell contact with Th1 cells expressing the target V gene. These findings indicate the potential of regulatory Th2 cells to inhibit not only the target Th1 cells, but also bystander Th1 cells expressing different V genes specific for other autoantigens. TCR peptide vaccines have been used in our studies to treat a total of 171 MS patients (6 trials), 484 RA patients (7 trials), and 177 psoriasis patients (2 trials). Based on this experience in 824 patients with autoimmune diseases, TCR peptide vaccination is safe and well tolerated, and can produce significant clinical improvement in a subset of patients that respond to immunization. TCR peptide vaccination represents a promising approach that is well-suited for treating complex autoimmune diseases.
    Neurochemical Research 07/2001; 26(6):713-30. DOI:10.1023/A:1010951706830 · 2.59 Impact Factor
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    ABSTRACT: We examined HIV-1 antigen specific intracellular expression of perforin on CD4+ and CD8+ lymphocytes in subjects with chronic HIV-1 infection on antiviral drug therapy after immunization with a gp120-depleted, whole killed HIV-1 immunogen (inactivated, gp120-depleted HIV-1 in IFA, REMUNE). Based upon previous results, we hypothesized that the restoration of adequate T helper immune responses by vaccination against HIV-1 could result in the augmentation of CD8+ lymphocyte immune responses measured as perforin expression. In the current study we observed an increase in the frequency of perforin in CD8+ lymphocytes in HIV infected individuals immunized with a gp120-depleted HIV-1 immunogen while on antiviral drug therapy. Furthermore, the frequency of HIV-specific CD8+ perforin expressing cells correlated with the T helper immune response as measured by the lymphocyte proliferative response (LPR). The induction of such responses with immunization may have direct antiviral consequences and is being studied in ongoing clinical trials.
    Clinical & Experimental Immunology 06/2001; 124(2):248-54. DOI:10.1046/j.1365-2249.2001.01534.x · 3.04 Impact Factor

Publication Stats

3k Citations
428.02 Total Impact Points


  • 2006
    • William Penn University
      Filadelfia, Pennsylvania, United States
  • 2005
    • Université de Sherbrooke
      • Division of Allergy Immunology
      Шербрук, Quebec, Canada
  • 1995–2002
    • Immune Design Corp.
      Seattle, Washington, United States
  • 2000
    • Vibra Hospital of San Diego
      San Diego, California, United States
  • 1998–2000
    • Mahidol University
      • Department of Pathobiology
      Siayuthia, Bangkok, Thailand
    • U.S. Army Medical Research Institute of Infectious Diseases
      Maryland, United States
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1999
    • Northwestern Memorial Hospital
      Chicago, Illinois, United States
  • 1985
    • University of Texas MD Anderson Cancer Center
      • Department of Clinical Immunology
      Houston, Texas, United States