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Abstract
It is difficult to summarize any discussion of a subject when it’s vitality and growth increase and change almost daily. It has been clearly demonstrated that the immune response is important in all organ systems of the body. The immunotherapy enters in each field of midicine. I am literally only scratching the surface of it’s complexity and applicability .
IN THIS WORK FOLLOWING HEADINGS WERE DISCUSSED:Cellular basis of the immune system and regulation of normal immune response.REGULATORY T-CELLS:
Regulatory T-cells (Treg) are in the focus of intense research in immunology, as reflected by the high number of primary research papers and reviews published nearly every week.
TYPES OF T REGULATORY CELLS:
Some Treg populations are naturally produced in the immune system as functionally distinct populations, while others are adaptively induced from naïve T-cells as a consequence of a particular mode of antigen exposure, especially in a particular cytokine milieu.
NATURALLY OCCURING T-REGULATORY CELLS:
Naturally occurring Treg (nTreg) cells compose 5–10% of peripheral T-cells, maintain a distinct lineage and develop in the thymus.
PERIPHERALLY INDUCED Treg CELLS:
The adaptive Treg cell subset includes type 1 Treg (Tr1) cells and T helper 3 (TH3) cells.
FOXP3: master control gene for the development and function of Tregs:
Recent notable findings are that the transcription factor Foxp3 is a key control molecule for Treg development and function and that a genetic anomaly of Foxp3, and the resulting deficiency or dysfunction of natural CD25+CD4+ Tregs.
TOLL-LIKE RECEPTORS AND IMMUNE REGULATION: THEIR DIRECT AND INDIRECT MODULATION ON REGULATORY CD4+ CD25+ T-CELLS
Recent studies have demonstrated that the immunosuppressive function of CD4+ CD25+ Treg cells can be regulated through TLR signalling. Various pathways, including the indirect route via APCs and their cytokine products as well as the direct effects of TLRs on CD4+ CD25+ Treg cells, may collectively contribute to the generation, expansion and function of CD4+ CD25+ Treg cells. Further studies are needed to clarify the molecular mechanisms for the regulation of CD4+ CD25+ Treg cells via TLRs.
IMMUNE REGULATION BY REGULATORY T-CELLS:
It is becoming increasingly clear that regulatory T-cells (Tregs) are equally important in inducing and maintaining peripheral self tolerance and thus preventing immune pathologies.
FUNCTIONAL charACTERISTICS OF NATURAL CD25+CD4+ TREGS AND THEIR MECHANISMS OF SUPPRESSION:
The suppression mechanism of activation-induced regulatory cells such as Tr1 cells is based primarily on the secretion of anti-inflammatory cytokines such as IL-10 and TGF-β.
CLINICAL APPLICATION OF REGULATORY T-CELLS:
The field of therapeutic application of Tregs in immune-mediated pathologies is at a very exciting crossroads.Clearly, many questions remain regarding optimization of strategies that target Tregs.
ROLE OF REGULATORY T-CELL IN TUMOR IMMUNITY:
Evidence from cancer patients suggests that increased Treg activity may be associated with poor immune responses to tumour antigens and contribute to immune dysfunction.
Treg CELLS IN HEMATOLOGIC MALIGNANCIES:
The first study by Marshall et al. demonstrated large populations of both IL10 secreting Tr1 and CD4+CD25+ Treg cells in Hodgkin’s lymphoma (HL) infiltrating lymphocytes and peripheral blood mononuclear cells (PBMC).
ROLE OF Treg CELLS IN AUTOIMMUNE DISEASES:
Accumulated evidence from the mid-1980s has shown that depletion of a particular T-cell subset from normal animals can cause autoimmune disease similar to the counterparts in humans, and that reconstitution of this subset can prevent these diseases. Subsequent detailed phenotypic characterisation of such autoimmune preventative cells now leaves no doubt of the existence of Treg cells as crucial mediators of self-tolerance in both animal models and humans.
MULTIPLE SCLEROSIS:
low cloning potential in the presence of IL-2, in Treg cells may allow for the over stimulation of CD4+ effector cells upon antigenic challenge, resulting in the production of proinflammatory cytokines and neuronal damage.
RHEUMATOID ARTHRITIS:
An increased frequency of Treg cells in directly related to reduced severity of RA. Thus, Treg cell proliferation and activity in the periphery and joints is essential for prevention of rheumatic disease and their dysfunction is implicated in pathogenesis.
TYPE-1 DIABETES:
Two methodologies have proven effective in the pursuit of utilizing Treg cells to prevent or reverse T1D.
ROLE OF Treg CELL IN ALLOGENEIC REACTIONS:
Graft rejection is mediated by the host immune system in response to the foreign graft cells. Dominant transplantation tolerance to BM and tissue grafts has been induced in mice. The presence or addition of Treg cells can induce antigen-specific tolerance to BM grafts, while reduction of Treg cells may accelerate GvHD and graft rejection.
ROLE OF Treg IN HEPATITIS C VIRUS INFECTION (HCV):
CD4+ CD25+ are known to be increased in patients with chronic hepatitis C but not in those who resolve the infection. Increase in Treg number and function, if present in the acute hepatitis phase of the infection, predicts a chronic evolution and persists over time.
THE ROLE OF Treg IN HUMAN IMMUNODEFICIENCY VIRUS(HIV) INFECTION:
progressive HIV disease has been associated with reduced frequencies or suppressor activity of CD25+ Treg cells in the peripheral blood.
Treg MONOCLONAL ANTIBODY:
Anti-CD25 monoclonal antibody injection results in the functional inactivation, not depletion, of CD4+CD25+ T-regulatory cells.