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Immunosuppressive Mechanisms (immunosuppressive + mechanism)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Treatment of alopecia areata with the 308-nm xenon chloride excimer laser: Case report of two successful treatments with the excimer laser

LASERS IN SURGERY AND MEDICINE, Issue 2 2004
Cuneyt Gundogan MD
Abstract Background and Objectives Alopecia areata is a common disease of unknown etiology; it causes significant cosmetic and psycho-social distress for most of the people it affects. We report on an innovative form of treatment in two patients with typical alopecia areata on the capillitium. Study Design/Patients and Methods We successfully treated two patients whose alopecia areata had worsened progressively for 3 and 14 weeks. The treatment involved the use of a 308 nm xenon chloride excimer laser (dosage 300,2,300 mJ/cm2 per session). Results After 11 and 12 sessions within a 9-week and 11-week period, the entire affected focus showed homogenous and thick regrowth. No relapse was observed during the follow-up period of 5 and 18 months. Conclusions The use of the excimer laser is an effective, elegant, and safe means of treatment and has good tolerability. Analogous to topical treatment of alopecia areata, the immunosuppressive mechanism of the excimer laser can be interpreted as an induction of T-cell apoptosis. This new means of treatment has yet to be discussed in medical literature. Further studies with greater numbers are needed to assess its potential more precisely and evaluate the excimer laser in treating alopecia areata. Lasers Surg. Med. 34:86,90, 2004. © 2004 Wiley-Liss, Inc. [source]

Signaling defects in anti-tumor T cells

IMMUNOLOGICAL REVIEWS, Issue 1 2008
Alan B. Frey
Summary: The immune response to cancer has been long recognized, including both innate and adaptive responses, showing that the immune system can recognize protein products of genetic and epigenetic changes in transformed cells. The accumulation of antigen-specific T cells within the tumor, the draining lymph node, and the circulation, either in newly diagnosed patients or resultant from experimental immunotherapy, proves that tumors produce antigens and that priming occurs. Unfortunately, just as obviously, tumors grow, implying that anti-tumor immune responses are either not sufficiently vigorous to eliminate the cancer or that anti-tumor immunity is suppressed. Both possibilities are supported by current data. In experimental animal models of cancer and also in patients, systemic immunity is usually not dramatically suppressed, because tumor-bearing animals and patients develop T-cell-dependent immune responses to microbes and to either model antigens or experimental cancer vaccines. However, inhibition of specific anti-tumor immunity is common, and several possible explanations of tolerance to tumor antigens or tumor-induced immunesuppression have been proposed. Inhibition of effective anti-tumor immunity results from the tumor or the host response to tumor growth, inhibiting the activation, differentiation, or function of anti-tumor immune cells. As a consequence, anti-tumor T cells cannot respond productively to developmental, targeting, or activation cues. While able to enhance the number and phenotype of anti-tumor T cells, the modest success of immunotherapy has shown the necessity to attempt to reverse tolerance in anti-tumor T cells, and the vanguard of experimental therapy now focuses on vaccination in combination with blockade of immunosuppressive mechanisms. This review discusses several potential mechanisms by which anti-tumor T cells may be inhibited in function. [source]

Enhancement of Immunogenicity of Jeg3 Cells by Ectopic Expression of HLA-A*0201 and CD80

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003
Serpil Koc
Problem: The choriocarcinoma cell line Jeg3 suppresses immunity in vitro by secretion of soluble factors like leukemia inhibitory factor suppressing leukocyte activation. The cells lack expression of classical human leukocyte antigen (HLA)-A and -B alleles but express some HLA-C, and non-classical HLA-G and -E. Upon binding to killing inhibitory receptor on natural killer (NK) cells, HLA-G prevents activation of cytolytic activity. We investigated whether Jeg3 cells are capable of immune stimulation after complementation with classical HLA and T cell costimulatory signal CD80. Method of study: Jeg3 cells were transduced to express HLA-A*0201 and/or CD80. Parental Jeg3 or transfectants Jeg3-A2, Jeg3-CD80 or Jeg3-CD80-A2 were used to stimulate allogeneic resting and activated peripheral blood lymphocytes (PBL). The different cell lines were loaded with a HLA-A2-restricted Epstein-Barr virus (EBV) recall antigen peptide epitope and antigen presenting ability was examined. T cell lines specific for Jeg3 and transfectants were generated from HLA-A2 matched and nonmatched donors and compared for expansion, phenotypes and cytolytic activity. Results: While all Jeg3 cell lines induced only marginal proliferation of resting T cells, phytohemagglutinin (PHA)-activated T cells were stimulated by CD80 or CD80-A2 expressing Jeg3. Only the transfectant Jeg3-CD80-A2 was capable of specific T cell stimulation by EBV recall antigen presentation. T cell lines of HLA-A2 non-matched donors stimulated with the Jeg3 transfectants showed significant expansion only when HLA-A2 and the costimulus CD80 were present. T cells from HLA-A2 positive donors did not expand significantly or differentially. No NK cells grew under any condition. In Jeg3-CD80-A2 stimulated T cells lines CD8+ cells expanded preferentially. These T cells exerted cytolytic activity toward all Jeg3 cell lines. Conclusion: Our data suggest that, in spite of immunosuppressive mechanisms, proliferative and cytolytic T cell responses are induced by Jeg3 cells when classical HLA- and/or costimulatory signals are present on the cells. [source]

Enhancement of immunogenicity of JEG-3 Cells by ectopic expression of HLA-A*0201 and CD80

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2002
Serpil Koc
The chorioncarcinoma cell line JEG-3 escapes immunity by secretion of leukocyte inhibitory factor suppressing leukocyte proliferation. The cells lack expression of classical HLA alleles but express nonclassical HLA-G, which binds to killer inhibitory receptor of natural killer cells, preventing cytolysis. We investigated whether JEG-3 cells are capable of immune stimulation after introduction of classical HLA and T-cell costimulatory signals. JEG-3 cells were transduced with vectors for HLA-A*0201 and/or CD80. Parental JEG-3, or JEG-3/A2, JEG-3/CD80, or JEG-3/A2/CD80 were used to stimulate allogeneic T cells. While parental JEG-3 cells induced only marginal proliferation of resting T cells, HLA-A2 or CD80 expressing JEG-3 induced enhanced proliferation. Double transfectants were most efficient. This difference was more obvious when T cells were preactivated by PHA. T cell lines restimulated with JEG-3 transfectants were characterized for expansion, phenotypes, and cytolytic activity. HLA-A2 matched and nonmatched donors were compared. T cells stimulated with JEG-3/A2 or JEG-3/CD80 were cytolytic towards parental JEG-3 cells. Again double positive JEG-3/A2/CD80 induced highest cytolytic activity, most obvious in HLA-nonmatched donors suggesting alloreactivity to HLA. Our data suggest that, in spite of immunosuppressive mechanisms, proliferative and cytolytic T cell responses are induced by JEG-3 cells when classical HLA and/or costimulatory signals are present on the cells. [source]