T cells are responsible for large number of functions that collectively result in cell mediated immunity (CMI). It is most effective in removing virus-infected cells, and also participates in defending against fungi, protozoans, cancers, and intracellular bacteria.
It also plays a major role in transplant rejection. Antigen- specific cytotoxic T-lymphocytes, macrophages, natural killer cells (NK) and various cytokines released in response to an antigen are involved in CMI.
Cellular immunity protects the body by:
1. Activating antigen-specific cytotoxic T-lymphocytes (CTLs) that are able to destroy body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens.
2. Activating macrophages and NK cells and facilitating them to destroy intracellular pathogens.
3. Stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses.
TH cells are involved in the selection of the effector mechanism to be directed against the selected target antigens.
Since activation of inappropriate mechanism results in enhanced susceptibility to the pathogens rather than protection, selection of effector mechanism is very important.
Even though cell mediated immunity strongly suggests the T cell dependent action, certain cell mediated immune reactions are T cell independent. Of course no cell mediated immune response is likely to occur in the total absence of T cells and antibodies.
Hence depending upon the involvement of T cells and antibodies cell mediated immunity can be classified in to (1) T cell independent (2) T cell dependent (3) antibody independent and (4) Antibody dependent cell mediated immunity.
T cell independent CMI:
Certain phagocytic NK cells kill and remove pathogens like bacteria and virus in the absence of T cells. The chemotactic factors released by the activated compliment system (Refer compliment system) or the cytokines released by the macrophages following activation through binding through antibodies draw phagocytic cells towards the pathogens and enhance their characteristic function.
For example TNFa released by the macrophages in response to the microbial components enhance the microbicidal activity of remaining macrophages, neutrophils, NK cells and K cells. In addition to that TNFa cause marginalzation and diapedisis of phagocytes to infiltrate the area of inflammation and phagocytose the pathogens.
The total reaction is T cell independent, different cells of immune system excluding T cells provide this immediate but non specific protection. This T cell independent CMI reaction may dependent on antibodies or may be independent of antibodies.
With reference to the role of antibodies it can be further divided in to antibody independent and antibody dependent T cell independent CMI.
(a) T cell independent, antibody dependent CMI:
Certain cells like K cells; eosinophils etc., have receptors for Fc region of antibodies. Through these receptors they fasten themselves to the antibody bound pathogens and kill the target cells by their cytotoxic action. Since antibodies are mediating this CMI reactions, this CMI is referred as “T cell independent antibody dependent CMI” and the immune cells involved in this reaction are considered as cytotoxic cells.
(b) T cell and antibody independent CMI:
Cells like natural killer cells and macrophages can kill the pathogen without the participation of antibodies. In this reaction enzymes of compliment system or the cytokines released by macrophages induce the cytotoxic action.
T cell dependent CMI:
Intracellular pathogens were removed by T cell dependent CMI. The effector T lymphocytes -TC, TD are responsible for this kind of CMI. Activated cytotoxic T cells bind to the target cell through MHC class I molecules present on the cell surface and cause lysis of the target cell.