The function of immune system degenerates in an aging-dependent manner and this results in immunosenescence. Human immune system includes two parts: genetic/innate immunity and adaptive immunity. The former is involved in monocytes, nature killer cells, and dendritic cells, the later is involved in acquired B and T lymphocytes. During the aging of immunity system, the both parts of immunity are damaged to some degree. Generally, innate immunity seems well-retained and the acquired immunity is degenerative seriously with aging. Immunocyte senescence is closely related to the elderly decreased ability to control infectious disease, cancer and to their generally poor response to vaccination. This review summarized the research progress on immunosenescence characteristics in aged phase.
Age Factors ; Aging ; immunology ; Antibody Formation ; immunology ; Cellular Senescence ; Humans ; Immunity, Cellular ; immunology ; Lymphocyte Activation

No abstract available.
Genetic Markers* ; Immunity, Cellular*

No abstract available.
Humans ; Immunity, Cellular* ; Lung*

Cell-mediated immune response is an important part of machinery in maintaining the body's homeostasis. After the innate immune system selectively activates the adaptive immune system, the cell-mediated immunity exerts its killing and clearance functions. Therefore, evaluating the level of cell-mediated immune response is crucial in the diagnosis and treatment of cancer, monitoring the immune status after organ transplantation, diagnosing and preventing viral diseases, and evaluating the effectiveness of vaccines and other areas. From the initial overall assessment of the immune effects in vivo to the precise detection of the number and function of multiple immune cells, the evaluation methods of cell-mediated immune response have greatly advanced. However, cell-mediated immune response involves multiple levels in the body, and it's difficult to choose the numerous detection methods available. The article systematically compares the evaluation methods of cell-mediated immune response at four different levels: the organism, the tissue and organ, the immune cells and the immune molecules, with the aim to facilitate the applications of related technologies.
Humans ; Immunity, Cellular ; Neoplasms/therapy* ; Immunity, Innate

No abstract available.
Glomerulonephritis, IGA* ; Immunity, Cellular* ; Immunoglobulin A*

No abstract available.
Glomerulonephritis, IGA* ; Immunity, Cellular* ; Immunoglobulin A*

Various immunologic investigations of 159 patients with Behqets syndrome undertaken included; the DNCB sensitization test, total T-cells and T-cell subsets and the lymphocyte transformation test using PHA. The percentage of positive esponsiveness to DNCB decreased in the order of possible (65%), suspected (60%), incomplete (37%) and complete type (37%), The number of patients with impaired LTT was larger in the group of patients with DNCB( + ) responsiveness (seventeen of 32) than in DNCB(+) group (six of 25), There was significant impairment of cell mediated immunity in Behcets syndrome compared to normal subjects, when analyzed by the impaired LTT and decreased proportions of helper T-cells.
Behcet Syndrome* ; Dinitrochlorobenzene* ; Humans ; Immunity, Cellular* ; Lymphocyte Activation ; T-Lymphocyte Subsets ; T-Lymphocytes ; T-Lymphocytes, Helper-Inducer

In our investigation, various immunologic aspects of 129 patients with complete and incomplete type of Behcet's syndrome were taken under consideration : quantitation of total T-cells by E-rosette method and B-cells by EAC-rosette method, helper/inducer T and suppressor/cytotoxic T-cells by monoclonal antibody technique(OKT4, OKT8), lymphocyte transformation test with PHA, quantitation of serum r-globulin by electro phoresis and quantitations of serum IgG, IgA, IgM, C3, C4 by immunodiffusion. From the results, the cell mediated immunity in Behcet's syndrome is not influenced by the number of patterns of four major symptoms or the activity of each major symptom at the time of test. However the humoral immunity is considered to be influenced by the above parameters.
B-Lymphocytes ; Behcet Syndrome* ; Humans ; Immunity, Cellular ; Immunity, Humoral ; Immunodiffusion ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulins* ; Lymphocyte Activation ; Lymphocytes* ; T-Lymphocytes

No abstract available.
Humans ; Immunity, Cellular* ; Lymphocytes* ; Tuberculosis, Pulmonary*

Effect of Mercury chloride on the synthesis of NO2- and ATP were observed in EMT-6 cells which were culture with cytokines(IL-1alpha and IFN-gamma) and various concentrations of mercury chloride from 0.05 to 0.08 M. Viability of EMT-6 cells were observed above 90% in almost groups. There were not significant differences in the viability between mercury supplemented groups and control group. It suggests viability of EMT-6 cells were not influenced by these concentrations of mercury chloride. Results of the synthesis of nitrite showed significant time and group effect. There is a significant interaction effect between concentration of mercury chloride and culture time. The effect of various concentration of mercury chloride is not the same for all levels of culture time. There were significant differences in the synthesis of nitrite between mercury chloride supplemented groups and control group, and the synthesis of nitrite in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. Results of the synthesis of ATP showed a significant group effect, and the time main effect and the Group x Time interaction were also significant. There were significant differences in the synthesis of ATP between mercury chloride supplemented groups and control group, and the synthesis of ATP in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. These results suggest that the disorder of cell mediated immunity by mercury chloride could be related to the inhibition of nitric oxide synthesis which will be caused by the decreased synthesis of ATP.
Adenosine Triphosphate* ; Immunity, Cellular ; Nitric Oxide