Cell-mediated immunity is involved in a variety of specific functions mediated by the T-lymphocyte.
The T-lymphocyte it so named because it passes through the thymus during the differentiation process, which leads to the mature T-cell.
T-lymphocytes do not carry typical immuno-globulins on their surfaces as do the B-cells.
However, they are functionally heterogeneous in that several subsets have been identified, including cytotoxic T-cells, memory T-cells, helper T-lymphocytes, and regulator T-lymphocytes.
Specific functions of T-lymphocytes include: protection against most viral, fungal and protozoan infections and slow-growing bacterial infections, such as tuberculosis, rejection of histoincompatible grafts, mediation of cutanoeus delayed hypersensitivity reactions, such as in tuberculin testing, and probably immune surveillance for malignant cells.
In addition, they also have regulatory functions within the immune system.
For example, helper T-lymphocytes assits B-lymphocytes and other types of T-cells to mount an optimum immune response.
The cellular immune response is initiated when a T-lymphocyte is sensitized by antigen.
In response to this contact the T-cell releases numerous humoral factors called lymphokines, which eventually bring about death of the antigen.
For example, chemotactic factor promotes the migration of phagocytes and other T-lymphocytes to the antigenic area, migratory inhibitor factor prevents their leaving the site, transfer factor transforms nonsensitized T-cells into sensitized T-lymphocytes, blastogenic factor initiates the rapid mitosis of sensitized T-cells, and macrophage activation factor transforms local macrophages to highly phagocytic cells.
Another lymphokin is interferon, which non-specifically inhibits viral replication, promotes phagocytosis, and stimulates the killer activity of sensitized lymphocytes.
The Immunologic properties of the mucosal lining of the gastrointestinal tract are immature, which predisposes this system, like the respiratory system, to increased risk of infection and inflammation.
The immunologic system undergoes numerous changes during the first year.
The newborn receives significant amounts of maternal IgG, which confers immunity for about 3 months against antigens to which the mother was exposed.
During this time the infant begins to synthesize his own IgG, and about 40% of adult levels are reached by adult levels are reached by 9 months of age.
The production of IgA, IgD, and IgE is much more gradual.
And maximum levels are not attained until; early childhood.
The defense mechanisms of the tissues and blood, particularly phagocytosis, are much more efficient in the toddler than in the infant.
The production of antibodies is well-established.
Immunoglobin G (IgG), which neutralizes microbial toxins, reaches adult levels by the end of the second year of Life.
Passive immunity from maternal transfer disappears by the beginning of toddler-hood, necessitating the use of artificial immunizations.
Immunoglobulin M (IgM), which responds to artificial immunizing techniques and combats serious infection, attains adult levels during late infancy.
Immunoglobins A, D and E increase gradually, not reaching eventual adult levels until later childhood.
Many young children demonstrate a sudden increase in colds and minor infections when entering nursery school or kindergarten because of the exposure to new antigens.
The T-lymphocyte it so named because it passes through the thymus during the differentiation process, which leads to the mature T-cell.
T-lymphocytes do not carry typical immuno-globulins on their surfaces as do the B-cells.
However, they are functionally heterogeneous in that several subsets have been identified, including cytotoxic T-cells, memory T-cells, helper T-lymphocytes, and regulator T-lymphocytes.
Specific functions of T-lymphocytes include: protection against most viral, fungal and protozoan infections and slow-growing bacterial infections, such as tuberculosis, rejection of histoincompatible grafts, mediation of cutanoeus delayed hypersensitivity reactions, such as in tuberculin testing, and probably immune surveillance for malignant cells.
In addition, they also have regulatory functions within the immune system.
For example, helper T-lymphocytes assits B-lymphocytes and other types of T-cells to mount an optimum immune response.
The cellular immune response is initiated when a T-lymphocyte is sensitized by antigen.
In response to this contact the T-cell releases numerous humoral factors called lymphokines, which eventually bring about death of the antigen.
For example, chemotactic factor promotes the migration of phagocytes and other T-lymphocytes to the antigenic area, migratory inhibitor factor prevents their leaving the site, transfer factor transforms nonsensitized T-cells into sensitized T-lymphocytes, blastogenic factor initiates the rapid mitosis of sensitized T-cells, and macrophage activation factor transforms local macrophages to highly phagocytic cells.
Another lymphokin is interferon, which non-specifically inhibits viral replication, promotes phagocytosis, and stimulates the killer activity of sensitized lymphocytes.
The Immunologic properties of the mucosal lining of the gastrointestinal tract are immature, which predisposes this system, like the respiratory system, to increased risk of infection and inflammation.
The immunologic system undergoes numerous changes during the first year.
The newborn receives significant amounts of maternal IgG, which confers immunity for about 3 months against antigens to which the mother was exposed.
During this time the infant begins to synthesize his own IgG, and about 40% of adult levels are reached by adult levels are reached by 9 months of age.
The production of IgA, IgD, and IgE is much more gradual.
And maximum levels are not attained until; early childhood.
The defense mechanisms of the tissues and blood, particularly phagocytosis, are much more efficient in the toddler than in the infant.
The production of antibodies is well-established.
Immunoglobin G (IgG), which neutralizes microbial toxins, reaches adult levels by the end of the second year of Life.
Passive immunity from maternal transfer disappears by the beginning of toddler-hood, necessitating the use of artificial immunizations.
Immunoglobulin M (IgM), which responds to artificial immunizing techniques and combats serious infection, attains adult levels during late infancy.
Immunoglobins A, D and E increase gradually, not reaching eventual adult levels until later childhood.
Many young children demonstrate a sudden increase in colds and minor infections when entering nursery school or kindergarten because of the exposure to new antigens.
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