L5 Flashcards
- Type I immune response (cellular).
- The activation phase begins when an antigen presenting cell (APC) encounters and attacks an invading virus.
- then , other viruses look for nearby cells, such as epithelial cells, to infect.
- A lysosome containing digestive enzymes combines with the phagosome to process the antigens
- The processed antigens combine with the MHC class II proteins and
presented on the surface of the APC. - The virus also infects the epithelial cells. Within the infected epithelial cell the virus is processed, attached to MHC class I protein and is presented on the cell surface.
- A helper T cell (CD4+) recognizes the displayed antigen on the APC and binds to the MHC class II-antigenic peptide complex.
- The activated helper T cell releases chemical messengers such as cytokine IL-2 and y-interferon
- The effector phase begins when activated cytotoxic T cell (CD8+), which were stimulated to proliferate by the cytokine IL-2, recognize the MHC class 1-antigenic peptide complex on the infected epithelial cells.
- The activated cytotoxic T cell binds to the MHC class I-antigenic peptide complex on the surface of the infected epithelial cells.
10 .The binding causes the cytotoxic T cell to release a potent chemical called perforin
11 .Perforin perforates the cell membrane of the infected cells causing the cells to lyse and die
12 .As the viral infection is brought under control, the activated cytotoxic T cells are turned off by regulatory T cells. - Memory T cells remain behind to respond quickly if the same virus attacks again
- Type II immune response (humoral).
1 Humoral immune response begins when an invading bacteria is phagocytized by antigen presenting cell (APC).
- A lysosome containing digestive enzymes combines with the phagosome to process the antigens.
- The processed antigens combine with the MHC class 2 proteins and are presented on the surface of the APC.
- Helper T cells (CD4) recognize the displayed antigen on the APC and bind to the MHC class 2-antigenic peptide complex.
- This binding triggers the APC to release the cytokine IL-1, which activates the helper T cell
- The activated helper T cell releases the cytokine IL-2, which stimulates the T cell to proliferate.
- Thus, producing many helper T cells, each with a receptor specific for the original processed antigen.
- The effector phase begins when a B cell that exhibits on its surface an IgM receptor specific for the same antigen originally engulfed by the APC encounters and binds the antigen.
- The B cell engulfs the complex by receptor-mediated endocytosis. The phagosome containing the antigen fuses with a lysosome. The antigen is processed
- The processed antigen binds MHC class II protein and is displayed on the surface of the B cell.
- Helper T cells now bind to the displayed antigen on the surface of the 8 cell causing the helper T cell to release cytokines.
- The cytokines stimulate the B cell to divide and proliferate into identical B cell copies.
- The cells differentiate (change and develope) into antibody producing plasma cells and memory cells.
- The plasma cells release antibodies with a specificity identical to that of the surface receptors on the parent 8 cell. These carry out the ultimate goal of fighting the foreign invaders.
- This makes it easier for killer cells to attack and destroy the bacteria by phagocytosis and the release of proteins causes the direct lyses of the bacteria
- Simultaneously a blood component known as complement is signaled to attack and puncture holes in the bacteria
- Age features of the immune system.
_Immunity during pregnancy . Because the fetus possesses antigens derived from its father ,and mother. , the fetus is consistently successful in establishing and maintaining itself through pregnancy, in spite of great histocompatibility difference. • The uterus is not a privileged site, since grafts of other tissues, such as skin, made in the uterine wall are readily rejected. Under some circumstances, the mother makes antibodies against fetal blood group antigens, and these can destroy fetal red blood cells either in utero, as in humans, or following ingestion of colostrum, as occurs in other mammals
- Aging and the Immune System Immunosenescence refers to the gradual deterioration of the immune system brought on by aging.
- Hematopoietic stem cells (HSC) diminish in their self-renewal capacity, —– reducing the supply of leukocyte progenitors. The number and function of phagocytes, natural killer (NK) dendritic cells decline with age. cells, and The functional capacity of T-cells declines with age
- Immune system in embryogenesis.
- Immune system in embriogenesis Maturation of the immune system starts early in fetal life
- Lymphocytes of the B series develop in the liver by 9 weeks’ gestation and are present in the blood and spleen by 12 weeks
- T lymphocytes start to leave the thymus from about 14 weeks
- phenotypes are present in the spleen
- development of secondary lymphoid tissues in healthy fetuses most probably reflects the lack of antigen stimulus.
- New born plasma contains adult levels of IgG which is acquired across the placenta from the mother.
- The small amounts of IgM (less than 20 mg dL) which are normally present in healthy newboms its include antibody with specificity lymphocytes.
- IgA synthesis normally starts in the secretory immune system, about 2-3 weeks after birth. Poor antibody responses by newborns following immunization, especially with bacterial capsular polysaccharides.
5-1 Immune system of newborns,
1) physiologically in new born immunodeficient, meaning innate and adaptive immunological responses are greatly suppressed. Early in life, the immune system is not mature enough to fight off pathogens and must depend on antibodies from the mother. Once born, a child’s immune system responds favorably to protein antigens and less so to glycoproteins and polysaccharides.
2) In neonates, opsonic activity and the ability to activate the complement cascade is very limited
3) Phagocytic activity is also greatly impaired in newborns. bcs the lower opsonic activity..
4) anyway the number of total lymphocytes in newborns is significantly higher than in adults, the cellular and humoral immunity is impaired.
5) Antigen-presenting cells in newborns have a reduced capability to activate T cells, work poorly and produce very small amounts of cytokines.
6) B cells develop early in gestation but are not fully active .
5-2 Immune system of, children,
- At birth, most of the immunoglobulin is present is maternal IgG. Because IgM, IgD. IgE and IgA don’t cross the placenta,
- they are almost undetectable at birth, although some IgA is provided in breast milk
- These passively acquired antibodies can protect the newborn for up to 18 months, but their response is usually short-lived and of low affinity
- By 6 to 9 months after birth, a child’s immune system begins to respond more strongly to glycoproteins. ง Not until 12 to 24 months of age
- the body’s response to polysaccharides. This information is used when developing vaccination schedules
5.-3 Immune system of adults,
During adolescence, the human body undergoes physical, physiological and immune changes, induced and mediated by various hormones. Females and males of puberty and post-pubertal age are at increased risk of developing autoimmune disorders. There is some evidence that cell surface receptors in B cells and macrophages may detect sex hormones in the system
5-4 Immune system of older persons.
at this time of the life of the human the immune system start getting effected by the ageing of the immune system
and the effect of immune system are manifest at multiple levels that include reduced production of B and T cells in bone marrow and thymus and diminished function of mature lymphocytes in secondary lymphoid tissues. As a result, elderly individuals do not respond to immune challenge as robustly as the young
