Question

Cytokines are regulatory proteins that act as signals between cells, creating a network for cell to cell signalling. Cytokines of the immune system are:

Interleukins which signal among leukocytes. At least 37 human IL have been identified.

Interferons (IFN) gamma IFN activated phagocytes and is secreted by T helper cells. Review the fucntion of IFN type I in chapter 15.

Growth factors stimulate leukocyte stem cells to divide and help with proliferation of certain cells of the immune system.

Tumor necrosis factor is secreted by macrophages and T cells to kill tumor cells.

Chemokines are chemotactic cytokines.

Be able to diagram an overivew of the immune system, include macrophages, eosinophils, basophils, neutrophils, natural killer cells, T helper cells, T cytotoxic cells and B cells. For each cell type include relevant information about receptors or markers on that cell's membrane.

B cells are lymphocytes that may differentiate into Plasma cells and memory cells. B cells have B cell receptors that bind to one Ag and each B cell has hundreds of BCR on its membrane surface. B cells also have a MHC I protein to present self Ag and a MCH II protein to present forgein Ag, or Ag that was able to bind that cell's BCR. Plasma cells have a great deal of RER and express antibodies. Memory cells are specialized to release IgG and are allowed to live a long cell life. The memory cells respond to a second contact with a given Ab by secreting large quantities of IgG within a few days of contact with the Ag.

T helper cells have a T cell receptor and a CD4 protien that work together to evaluate foreign Ag presented in MHC II proteins by antigen presenting cells. B cells and macrophages are examples of Ag presenting cells. T helper cells may release cytokines to stimulate B cells to proliferate and differentiate into memory cells and plasma cells. T helper cells would also have MHC I to present self Ag.

T cytotoxic cells also have a T cell receptor and CD8 protein to evaluate Ag presented in MHC I proteins. T cytotoxic cells identify tumor cells or virally infected cells by recognizing altered self Ag presented in a given cell's MHC I protein. T cytotoxic cells also have two modes of killing a target cell, the perforin-granzyme pathway and the CD95 pathway. p.487

5. Name one other cell of the immune system that utilizes perforin -granzyme pathway and explain how that cell's use differs from a T cytotoxic .

6. Does a T helper cell directly kill a foreign cell or a virally infected cell? What is the role of a T helper cell in the immune system?

7. HIV lowers a person's T helper cell count. What effect would a very low T helper cell count have the immune system function?

T regulatory cells moderate T cytotoxic cell activity. Cell mediated responses must be regulated to reduce the possibility of autoimmune responses.

8. Describe how graft rejection involves T cytotoxic cells. p532

The primary immune response to an antigen is slow, the antibodies are synthesized by plasma cells which take days of cell division to develop. The IgM antibodies may be in the serum in 7-10 days from the initial contact.

9. If the bacteria is releasing a toxin that within hours, will the body be able to make antibodies to neutralize the toxin within hours? How long might it take? How can that person acquire immunity quickly?

When an Ag is encountered for the second time, the activation of memory cells ensures the production of Ab for that Ag is fast and at high concentration is the serum.  

10. The flu virus mutates its Ag quickly, does having the flu one season confer immunity through memory cells for the next season? If so why, if not why not?

Answer 1

5. T-cytotoxic and NK cells both induce programmed cell death in target cells. Perforin-granzyme pathway is also expressed in other types of immune cells such as dendritic cells, B cells and mast cells. They are also expressed in non-immune cells like keratinocytes, pneumocytes and chondrocytes.

But these cell types differ from cytotoxic T cells as they either do not express perforin or do not form immunological synapses. Granzyme B is released extracellularly. Extracellular granzyme B can accumulate in the extracellular space.

6. Helper T-cells do not kill the viral infected or foreign cells directly. They are important in adaptive cell immunity as they are required for almost all adaptive immune response. They activate B-cells to secrete antibodies and macrophages to destroy ingested microbes. They also activate cytotoxic T-cells to kill the infected target cells.

7. HIV lowers person's T-helper cells. The p[rogressive decreases in the number of helper T-lymphocytes in the body of the infected person, leads to a number of infections that could have been otherwise overcome such as those due to bacteria especially mycobacterium, viruses, fungi and even parasites like Toxoplasma.

8. Rejection is an adaptive immune response via cellular immunity mediated by killer T-cells inducing apoptosis of target cells as well as humoral immunity mediated by activated B-cells secreting antibody molecules.

Cytotoxic CD8 T-cells can effect graft rejection autonomously. CD8 T cells could escape from immunosuppression and participate in the rejection process.

9. If bacteria enter into the body the macrophages and neutrophils of innate immunity provide first line of defence which is immediate. However they always cannot eliminate infectious organisms and there are pathogens that they can =not recognise. When the bacteria produce toxins, the adaptive immune response comes into action. It is the response of antigen-specific lumphocytes to antigen.

There is a delay of 4-7 days before the initial adaptive response takes effect. The innate immune response has a critical role in controlling infection during this period.

For quick immunity when the body has to be provided with ready made antibodies as in passive immunity.

Aquired immunity is pathogen specific. it is characterised by memory. This means that our body when encounters a pathogen for the first time produces a response called primary response which is of low intensity. Subsequent encounter with the same pathogen elicits a highly intensified secondary or anamnestic response. This is because the body has the memory of the first encounter.

10. The flu virus mutates very fast. When the flu virus enters the body first time, the body responds to it and it will have memory cells. But as the flu virus mutates very fast, when the body encounters with flu virus again, the body 's memory cells fails to recognise, leaving the vuirus free to infect us once more. So with each flu attack the immune system becomes resistant to the virus that caused it.