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J J Ellner

Publications and source records attributed to J J Ellner.

225 records · Page 13Linked to original sources

Phytohemagglutinin-induced proliferation of guinea pig thymus-derived lymphocytes. II. Accessory cell function.

Accessory cell participation in PHA-induced thymus-derived lymphocyte DNA synthesis encompasses two distinct functions. The first consists of maintenance of the functional integrity of resting lymphocytes, and the second involves the direct induction and/or support of T cell proliferation in response to this mitogen. Whereas the reducing agent 2-mercaptoethanol can support an Mphi-depleted population of resting lymphocytes so that the latent biologic activity is maintained, it is not itself sufficient to allow the induction of lymphocyte proliferation in response to PHA. This latter function requires intact accessory cells.

Animals↗

Quantitative and immunologic aspects of the handling of 2,4 dinitrophenyl guinea pig albumin by macrophages.

Studies correlating quantitative aspects of the handling of dinitrophenyl guinea pig albumin (DNP-GPA) by guinea pig macrophages with the potential of cell-associated antigen to initiate proliferation of immune T lymphocytes have examined the nature of immunologically relevant antigen. After the loss of 75% of cell-bound DNP-GPA during the first 24 hr of in vitro culture, the remaining antigen persists qualitatively unchanged throughout further culture. However, coincident immunogenicity of the macrophage-associated NDP-GPA progressively deccreases, suggesting loss of accessibility of the antigen to responding immune lymphocytes. There is a small, stable, surface antigen pool but these studies suggest that the immunologically critical fraction of DNP-GPA, as regards guinea pig T cell activation, is resistant to trypsinization and inaccessible to antibody.

Animals↗

Immunologic aspects of mycobacterial infections.

Immunosuppressive mechanisms loom as important factors in depression of delayed-type hypersensitivity responses during active tuberculosis. Nonspecific suppression may be mediated by circulating immune complexes containing mycobacterial polysaccharides such as D-arabino-D-galactan. The mechanism of suppression involves activation of monocyte production of immunosuppressive prostaglandin E2. Peripheral blood mononuclear cells from patients with tuberculosis include increased numbers of monocytes that suppress the response to tuberculin purified protein derivative (PPD). Antigen-specific suppression is associated with monocyte activation by a number of criteria, including decreased surface expression of HLA-DR determinants and increased production of interleukin 1 (IL-1). The increased production of IL-1 is associated with--and may have a causal relation to--immunosuppression. A second parallel regulatory mechanism involves PPD-specific suppression by Fc gamma receptor-bearing lymphocytes. The consequence of these immunosuppressive circuits is depression of tuberculin-induced blastogenesis, production of IL-2, and generation of IL-2 receptors. These findings suggest that natural infection with Mycobacterium tuberculosis may result in immunosuppression. Studies of potentially protective antigens in experimental systems must be designed to assess and avoid activation of suppressor circuits.

Antibodies, Monoclonal↗

Septic arthritis caused by Bacteroides fragilis.

As improvements in bacteriologic techniques have enhanced the recovery of anaerobic bacteria from clinical specimens, there has been an increasing awareness of the role of anaerobes in disease. Bacteroides fragilis is the most common anaerobic organism found in clinical specimens. Although it is the anaerobe most frequently associated with bacteremia and a common isolate in intraabdominal infections, infections of the female genital tract, wounds, and abscesses, B. fragilis is a rare cause of septic arthritis. The isolation of this organism from four patients with septic arthritis in three Cleveland hospitals between 1978 and 1982 suggests that septic arthritis due to B. fragilis may be a more common clinical entity than previously appreciated. In this report we describe these cases and review the pertinent literature.

Adult↗

Risk factors for HIV infection in homosexual men: the Cleveland men's study of risks in a low-prevalence area.

Detailed questionnaires concerning alcohol and drug use, sexual practices, and medical history were completed by 301 homosexual men living in the Cleveland metropolitan area. Their sera were subsequently tested for antibodies to the human immunodeficiency virus. Fifty-six (18.6%) were seropositive. In a univariate analysis, age, drug use, and four specific sexual practices were associated with seropositivity. In a multiple logistic regression analysis, intravenous drug use and receptive anal-genital sex remained independent predictors of seropositivity.

Adolescent↗

Regulation of the human cellular immune response to Mycobacterium tuberculosis. The mechanism of selective depression of the response to PPD.

After infection with M. tuberculosis, about 5% of individuals develop progressive tuberculosis during the following two years and an additional 5% delayed reactivation. The genetic and acquired factors which place individuals at risk of tuberculosis are partly defined; however, the connection of the susceptibility to the host immune response is much less clear. Recent studies have examined the basis for the immunosuppression that is a concomitant of tuberculosis. Direct stimulation of monocytes primed during the course of tuberculous infection by mycobacterial peptides appears to be responsible for suppression of PPD-induced responses. Increased expression and release of interleukin-2 receptors and transforming growth-factor beta are associated with and may contribute to such suppression by monocytes. Additional studies have addressed the generation of immunity or immunosuppression. Ingestion of live M. tuberculosis by monocytes leads to selective expansion of gamma-delta T cells as opposed to CD4 lymphocytes. This may be relevant to the innate response to infection with M. tuberculosis as well as immunoregulatory circuits. Increased understanding of the basis for immunosuppression is of intrinsic interest as regards regulation of specific pathways of immune reactivity in an infectious disease of humans and may provide some insight into factors predisposing to tuberculosis.

Humans↗

Measurement and partial characterization of an interleukin-2 inhibitor (IL-2-IN) in human urine.

We observed a human urine-derived protein complex (IL-2-IN) which competitively inhibits interleukin-2 (IL-2) dependent murine lymphocyte proliferation. Measurements of urinary IL-2-IN have been used to stratify the immune response of patients to bacteria in the bladder. Partial characterization of IL-2-IN indicates that it is a heat-stable, 75 kDa complex comprised of interleukin-2 bound to another protein(s). Although the IL-2-IN complex is stable in physiologic buffers, the complex can be disrupted using acidic or low-ionic strength buffers, thereby liberating IL-2. IL-2-IN activity is susceptible to bacterial and endogenous urinary proteolysis. The IL-2 bound in the IL-2-IN complex cannot be detected using a double monoclonal antibody radioimmunoassay for IL-2. Unlike other IL-2 binding proteins, the IL-2 binding protein of the IL-2-IN complex is not a soluble interleukin-2 receptor. A modification of the bioassay for interleukin-2 activity is the method of choice for the detection and quantification of urinary IL-2-IN.

Chromatography, Gel↗