1- How are humoral and cell-mediated immunity different from each other and what types of “invaders” do they each typically destroy? 2- List AND describe 3 ways that antibodies can inactivate foreign cells or substances. 3- Describe the steps involved in activating a specific immune response and how primary and secondary immune responses differ, Be sure to include in your answer how the clonal selection mechanism operates 4- Use an example to describe how endocrine control systems work and how the hypothalamus is related to the anterior pituitary and a peripheral endocrine gland, like the thyroid, adrenal cortex, or gonad 5- Choose an example of a hormone (e.g. epinephrine) that uses either CAMP or Ca++ as a second messenger. What are the stimuli for the release of the hormone? What are the steps in the process of changing what a target cell is doing? Give a specific example of a process that is changed in the target cell after the cell receives the hormone signal.

QUESTION

1- How are humoral and cell-mediated immunity different from each other and what types of “invaders” do they each typically destroy?

2- List AND describe 3 ways that antibodies can inactivate foreign cells or substances.

3- Describe the steps involved in activating a specific immune response and how primary and secondary immune responses differ, Be sure to include in your answer how the clonal selection mechanism operates

4- Use an example to describe how endocrine control systems work and how the hypothalamus is related to the anterior pituitary and a peripheral endocrine gland, like the thyroid, adrenal cortex, or gonad

5- Choose an example of a hormone (e.g. epinephrine) that uses either CAMP or Ca++ as a second messenger. What are the stimuli for the release of the hormone? What are the steps in the process of changing what a target cell is doing? Give a specific example of a process that is changed in the target cell after the cell receives the hormone signal.

ANSWER

Humoral and cell-mediated immunity are two different components of the immune system that work together to defend the body against pathogens. 

Humoral immunity involves the production of antibodies, which are proteins produced by B cells (a type of white blood cell). Antibodies circulate in the blood and other bodily fluids, targeting and neutralizing pathogens such as bacteria and viruses. They can bind to antigens on the surface of these invaders, marking them for destruction by other immune cells or by activating the complement system. Humoral immunity is particularly effective against extracellular pathogens.

On the other hand, cell-mediated immunity involves the action of T cells, another type of white blood cell. T cells recognize and directly destroy infected cells, as well as play a role in regulating the immune response. This type of immunity is important in combating intracellular pathogens such as viruses and certain types of bacteria. T cells can also help activate B cells to produce antibodies.

Antibodies can inactivate foreign cells or substances through several mechanisms:

 Neutralization: Antibodies can bind to viruses or bacterial toxins, preventing them from attaching to host cells and neutralizing their harmful effects (Klimpel, 1996). By binding to the pathogen, antibodies can prevent it from entering host cells and causing infection.

Opsonization: Antibodies can coat the surface of bacteria or other pathogens, marking them for destruction by phagocytic cells such as macrophages and neutrophils. This process enhances the recognition and engulfment of the pathogen by these immune cells.

Complement activation: Antibodies can activate the complement system, which is a group of proteins that help destroy pathogens. When antibodies bind to a pathogen, they can trigger a cascade of complement protein activation, leading to the formation of a membrane attack complex that punches holes in the pathogen’s cell membrane, causing it to burst.

 The process of activating a specific immune response involves several steps

Recognition: Immune cells, such as B cells and T cells, recognize specific antigens present on pathogens. B cells have surface receptors that can directly bind to antigens, while T cells recognize antigens displayed by infected cells or antigen-presenting cells.

Activation: Once recognized, immune cells are activated. In the case of B cells, activation involves the binding of the antigen to its surface receptor, which triggers a series of signaling events leading to the production of antibodies (Janeway, 2001). For T cells, activation requires interaction with antigen-presenting cells and the recognition of specific antigen fragments displayed on their surface.

Clonal selection: During activation, a specific subset of B or T cells with receptors that can recognize the antigen is selected for proliferation. This process, known as clonal selection, ensures the generation of a large number of effector cells that can target the invading pathogen.

 Effector response: The activated B and T cells differentiate into effector cells that carry out the immune response. B cells differentiate into plasma cells that secrete large amounts of antibodies, while T cells differentiate into cytotoxic T cells that directly kill infected cells or helper T cells that regulate the immune response.

Primary and secondary immune responses differ in terms of speed and magnitude. The primary immune response occurs when the immune system encounters an antigen for the first time (Chaplin, 2010). It takes several days for the immune system to mount an effective response, as it needs time to recognize the antigen, activate specific cells, and generate a sufficient number of effector cells. 

In contrast, the secondary immune response occurs upon re-exposure to the same antigen. It is faster and more robust due to the presence of memory cells, which are long-lived cells that “remember” the antigen from the initial encounter. Memory B cells can rapidly differentiate into plasma cells, leading to a faster and higher antibody production. Memory T cells can quickly recognize and eliminate infected cells, providing a more rapid and effective immune response.

Endocrine control systems involve the communication and regulation of bodily functions through the secretion and action of hormones. An example of how the hypothalamus is related to the anterior pituitary and a peripheral endocrine gland is the hypothalamic-pituitary-thyroid axis.

The hypothalamus releases thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH). TSH then acts on the thyroid gland, stimulating the release of thyroid hormones, including thyroxine (T4) and triiodothyronine (T3). These thyroid hormones have widespread effects on various body tissues, influencing metabolism, growth, and development.

The hypothalamus regulates the release of TSH from the anterior pituitary through a negative feedback loop. When the levels of thyroid hormones in the bloodstream are sufficient, they inhibit the release of TRH and TSH. Conversely, when thyroid hormone levels are low, the hypothalamus senses this and increases the release of TRH, which stimulates the anterior pituitary to release TSH, ultimately leading to the production and release of thyroid hormones by the thyroid gland.

An example of a hormone that uses cAMP (cyclic adenosine monophosphate) as a second messenger is epinephrine (also known as adrenaline). Epinephrine is released by the adrenal glands in response to stress or excitement.

The stimuli for the release of epinephrine include physical or emotional stress, exercise, or danger. These situations activate the sympathetic nervous system, triggering the release of epinephrine into the bloodstream.

Once epinephrine binds to its receptor on the surface of target cells, it activates a G-protein-coupled receptor. This receptor then activates an enzyme called adenylyl cyclase, which converts ATP (adenosine triphosphate) into cAMP. cAMP acts as a second messenger, relaying the signal from the epinephrine receptor to the cell’s interior.

The increased levels of cAMP inside the target cell initiate a cascade of intracellular events. cAMP activates protein kinase A (PKA), an enzyme that can phosphorylate target proteins. Phosphorylation by PKA can alter the activity of various enzymes and proteins, leading to changes in cell function.

For example, in liver cells, epinephrine stimulates the breakdown of glycogen (glycogenolysis) into glucose, increasing blood sugar levels. Epinephrine activates PKA, which phosphorylates enzymes involved in glycogen breakdown, thereby promoting the release of glucose from liver cells into the bloodstream. This process provides a rapid source of energy for the body during times of stress or physical exertion.

References

Chaplin, D. D. (2010). Overview of the immune response. The Journal of Allergy and Clinical Immunology, 125(2), S3–S23. https://doi.org/10.1016/j.jaci.2009.12.980 

Janeway, C. A., Jr. (2001). B-cell activation by armed helper T cells. Immunobiology – NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK27142/ 

Klimpel, G. R. (1996). Immune Defenses. Medical Microbiology – NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK8423/