On The Role Of T-cell Subsets And Cytokines In The Pathogenesis Of Systemic Lupus Erythematosus

Autoimmune diseases are diseases caused by internal and external factors when the body's own immune system overreacts or is out of control and undermines the body's own organs directly or indirectly, and cause corresponding organ pathological changes or clinical symptoms. There are many dysimmunities in auto-immune disease patients, especially T-cell subset disproportion: Th1 and Th2 cell's proportion is disequilibrium; reactively. T-cell proliferation; active B-cell cells to produce ponderosus autoantibody; damage in the patient's immune system lead to immune function disorder, provoke the autoimmune disease.Systemic lupus erythematosus (SLE) is a typical autoimmune disease, which causes damages in many body systems and organs. It has as its feature the activation of polyclonal B-cells and the production of many autoantibodies. It is a chronic inflammation of connective tissue brought about by genetic, hormonal and environmental factors. It's already been realized that the over actived B-cell which produce the pathogenicity autoantibody is T-cell dependent in immunoloregulation component element, and supposed that there is the Th-cell subset disequilibrium in the SLE patients, but the basic feature of the Th-cell subset disequilibrium is still not clear. At present, it's still controversy about the Th1 or the Th2 immune response, which is the primary in SLE. There is no final conclusion about the express level of various kinds of cytokine in SLE patients or in animal models. At present therer are three viewpoints about the SLE patient Th subgroup unbalancedly, including the Th1 superiority, Th2 superiority and Th1 to Th2 superiority transformation.The experiment measures the sera of patients with SLE autoantibody levels and immunofluorescence pattern, serum circulating immune complexes, C-reactive protein, immunoglobulin, complement content of peripheral blood mononuclear cells in patients with the secretion of IL-2 and IFN-γ, IL-4 cytokines levels and in vivo expression from the mRNA level and cell level. The aim of this experiment is to study the role of the T cell subgroup and the cytokine in the SLE morbidity process, the type of the immunologic function disorder. We analyze the characteristic of the Th cell subgroup disequilibrium, discuss its immunity pathogenesis, and to provide the reference for the SLE diagnosis, monitor of its activity and the prognosis appraisal. In this experiments the SLE patient's blood serum contains many kinds of autoantibody, mainly includes anti-nuclear antibody (ANA), anti- double- stranded DNA(ds-DNA) antibody, anti-Smith(Sm) antibody, among the total, the dsDNA is obvious related to the reactiveness of this disease, it is the specificity antibody of the SLE. The highly concentrated C response protein in the serum demonstrates the SLE patient immunologic function disorder, infects concurrently easily, and correlates with disease's activity. The circulation immune complex CIC quantity obviously increase, it settles in the organization and may activate the complement, causes the inflammation harm, and further causes autoantibody released, make the course of SLE procrastinates, unceasingly aggravates. The immunoglobulin elevation which the literature reported has not been manifested in this paper, but the decreased complement content confirms that the complement system's activation and immunologic function damage exist in SLE patients. Several different methods are used to examine the expression level of SLE patient's cytokine IL-2, IFN-γ, the IL-4. All these findings prompt that the immunity adjustment barrier and the immunologic dysfunction exist in vivo the SLE patients, include the Th subgroup dysfunction, unbalanced proportion, balanced deviation, Th1/Th2 functional disorder, Th2 function hyperfunction, but the Th1 function is insufficient, thus causes in vivo cytokine proportion to be unbalanced, excessive activation of B cells, produces a variety of autoantibodies, and causes organism immunologic function damage. All these factors contribute to the abnormality of the cellular immunity and the humoral immunity, the immunological regulation function disorder, and causes autoallergic disease.In summary the T cell subgroup, especially Th subgroup cytokines are playing the vital role particularly in the SLE morbidity. SLE patients in vivo not only have the high activation of B lymphocyte's, the T lymphocyte is also activated, together with other response cells to produce avariety of biological activity factors, and forms the complex immunity regulating network to control the immune response system. Autoimmune disease is caused by inordinate activates immune response which is mediated by the active T cell and the cytokines. The main abnormality of the immune system is the hyperfunction of T-cell-dependent B cells, produce the massive autoantibodies and the immune complex, the cytokine imbalance and cytokine spectrum displacement is obvious existence in its morbidity.The pathogenesis of auto-immune disease is very complex. The abnormality of variety of cytokines may simultaneously exist in one patient, thus we cannot isolate regard abnormality of one kind of cytokine, and cannot simply consider that the reduced cytokine has the protective function, and the elevated cytokine has the pathogenesis function. The interaction of many kinds of cytokine is possibly more important. Although the SLE research already entered the cell and molecular level, but the accurate pathogenesis of SLE is still not clear. At present, the possible pathogenesis of the SLE is that the patients who have the hereditary predisposition are influenced by the environmental factor and/or sex hormone, to induce the abnormal immune response. The B cells are excessively activated, and produce massive pathogenic autoantibodies and immune complexes. The impairment of immunoloregulation mechanism, the loss of the immune tolerance, the antigen load increases, the excessive helper T cell and the impairment of B cell inhibition cause one kind or several kinds of cytokine abnormality expression. Th1 cells transform to the Th2 cell and lead to cytokine network imbalance, which finally caused the SLE.