The process of multipotential lymphatic stem cell maturation and differentiation into immunocompetent T cells is accomplished by the expression and deletion of specific surface CD antigens. The CFU-Lstem cells enter the medulla of the thymus via a post capillary venule and then migrate to the periphery of the thymic lobule. The presence of CD2 and CD7 molecules on the cell surface indicates an early stage of differentiation. This is followed by expression of the CD1 molecule, indicating the midstage of Tcell differentiation. As maturation progresses, the cells express TCRs, CD3, CD4, and CD8 molecules. It seems that intensity of interreacion between TCR/co receptor molecule complex and self peptide/MHC complex determine the outcome of the thymocite selection process. If the lymphocyte recognizes self MHC and self or foreign antigen, it will survive the selection (positive selection); if not, death of the cell will occur. Cells that pass the positive selection test leave the cortex and enter the medulla. Here they undergo another selection process in which cells directed to selfantigen displayed by self MHC are eliminated (negative selection). Cells that survive that selection then become either cytotoxic CD8+ Tlymphocytes or helper CD4+ Tlymphocytes.

Periodontal disease is a chronic inflammatory disease that is largely attributable to infections with gram-negative bacteria and is characterised by both gingival inflammation and alveolar bone resorption. Beside macrophages, the second most common cells of the gingival inflammatory infiltrat are mast cells. Mast cells are heterogenous cell population which live from six months to one year. These cells are activated by differnt immunologic and non-immunologic signals. Activated mast cells can secrete a range of substances that regulate angiogenesis, tissue remodeling and wound healing, which include both degradation and synthesis of tissue components. Apart from that, mast cells have an important role in phagocytosis, antigen processing and presentation to T-cells. It is confirmed that gingival mast cells can express matrix metalloproteinases (MMPs) and the tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2. This indicates that mast cells are likely to play an important role in inflammation and tissue degradation in periodontal diseases.

Dendritic cells (DCs) are antigen presenting cells which trace origin from bone marrow cells. These cells are discovered and described by Steinman i Cohn (1973) in peripheral lymphoid organs of mice. The cellular membrane of DCs are place of expression of plenty immunoregulatory molecules such as MHC class I and II, co stimulatory, and adhesion molecules, as well as many receptors for different cytokines. Armed on this way, DCs are one of the most effective antigen presenting and immunoregulatory cells. Moreover, role of DCs in development of immune reaction can be crucial due to they are one of the most important cellular “link” between native and adaptive immunity. DCs are engaged in mechanisms of antigen processing and presentation, induction of immune reaction, establishing immune tolerance and immune reaction regulation, balancing the immune reaction between autodestruction and protection of “self” cells. These functions makes that DCs play very important role in development of some pathological conditions and diseases such as autoimmunity, allergies and quality of anti-tumor and anti-microbe defense. Unbalanced immune reaction is hallmark of all cited diseases and immunopatological conditions, so that the function of DCs should be explored on the better way.

Adipose tissue secretes bioactive peptides, termed 'adipokines', which act locally and distally through autocrine, paracrine and endocrine signals. Those signals influences the answers of other tissues and organs including hypothalamus, pancreas, liver, sceletal muscles, endotel an immune system. Increased production of most adipokines impacts on multiple functions such as appetite and energy balance, immunity, insulin sensitivity, angiogenesis, blood pressure, lipid metabolism and haemostasis, all of which are linked with cardiovascular disease. Leptin is a critical mediatorof energy balance that relays information regarding the depletion or accumulation of fat stores to the brain. Althoughmany of leptin's effects result rb from a direct action ofleptin on hypothalamic neurons, the functional leptin receptor(long-form or lep ) is also found on many tissues outside the central nervous system (CNS), including immune cells. Obese individuals seem to be resistantto the hypothalamic effects of leptin (maybe because of defective blood-brain barrier transport), the catabolic pathways designed to reduce appetite and increase energy expenditure are not activated and excess body weight is maintained). Adipokines like adiponectin and leptin, at least in physiological concentrations, are insulin sparing as they stimulate beta oxidation of fatty acids in skeletal muscle. The role of resistin is less understood. It is implicated in insulin resistance in rats, but probably not in humans. Adiponectin and resistin are adipocyte-derived polypeptide hormones playing a role in metabolic homeostasis. Their plasma levels are inversely (adiponectin) or directly (resistin) correlated to obesity (and in a patients with type 2 diabetes mellitus) and they have opposite effects on insulin sensitivity. Adipocytes secretes also adipsin, factor B and factor C. In-depth understanding of the pathophysiology and molecular actions of adipokines may, in the coming years, lead to effective therapeutic strategies

In regulation of specific immune responses the most important role play interleukin-2, IL-4, IL-5, IL-13, inter feron- (INF- ), transforming growth factor- (TGF- ) and lymphotoxin (LT). These signal molecules are produced mainly by T-lymphocytes after recognition of foreign antigens by specific receptors (TCR) placed on plasmalema. Some of mentioned cytokines stimulate proliferation and differentiation of various lymphocyte populations in the activation phase of T cell-de pendent immune responses, while the others activate and regulate the function of specialized effector cells, such as mono nuclear phagocytes, eosinophils, and neutrophils, to eliminate antigens in the effector phase of immune responses. In con trast to most of cytokines which have stimulating action on an initiation and course of humoral and cell-mediated immune responses, TGF- has an inhibitory effect on the activation and proliferation of T-lymphocytes and the other leukocyts

The complement system (complement) involves over 30 circulating and membrane-fixed proteins with an effector
role in the innate and humoral immunity. These proteins help the function of antibodies to protect the organism from foreign
molecules (antigens) which the term complement comes from. Soluble proteins of the complement system made mainly in
the liver and circulate in blood in an inactive form. The activation of complement may be initiated in three ways (classical,
alternative and lecitin pathway), and it is realized by sequential proteolysis of complement proteins (proenzymes) which
become emzymes with the proteolitic activity after cleavage. Products of the activatin of complement bind to the surface of
microbes or to the antibodies bound to antigens. An activated complement shows a number of biological effects, such as
lysis of an attached cell, opsonization, neutralization of viruses, inflammation, clearance of immune complexes etc. In contrast of microorganisms, human cells have a number of regulatory proteins which prevent the complement activation and in that way, they regulate its activity