Question

1. Describe the 3 levels of defense mechanisms.
2. Describe the importance of mast cells, complementary proteins and phagocytes in inflammatory response.
3. Why is the lymphatic system important for the immune system?

Please, type the answers

Answer 1

ANSWER 1) THE THREE LEVEL OF DEFENSE MECHANISM ARE:

• The first line of defense in our bodies are physical and chemical barriers - our skin, stomach acids, mucus, tears, vaginal opening, of which the last three mostly produce lysozyme to destroy harmful incoming pathogens.
• In our bodies the second line of defense is non-specific immune responses - macrophages, neutrophils, interferons, and complement proteins. This line of defense also includes fever and inflammatory response as nonspecific defenses.
• Our third line of defense is specific immune responses - T Cells and B Cells. There are many types of each which work like a close knit team to destroy pathogens.

If pathogens (invaders) try and succeed in penetrating the first line of defense, then the second line of defense is ready to act. If both the first and second line of defense fail, then the third line of defense will act. It is when all three lines of defense are breached that we get sick and are subject to disease.

ANSWER 2 ) Inflammation is the immune system's response to harmful stimuli, such as pathogens, damaged cells, toxic compounds, or irradiation, and acts by removing injurious stimuli and initiating the healing process. Inflammation is therefore a defense mechanism that is vital to health. Usually, during acute inflammatory responses, cellular and molecular events and interactions efficiently minimize impending injury or infection

At the tissue level, inflammation is characterized by redness, swelling, heat, pain, and loss of tissue function, which result from local immune, vascular and inflammatory cell responses to infection or injury. Important microcirculatory events that occur during the inflammatory process include vascular permeability changes, leukocyte recruitment and accumulation, and inflammatory mediator release.

Mast cells are well known for their role in allergic and anaphylactic reactions, as well as their involvement in acquired and innate immunity. Increasing evidence now implicates mast cells in inflammatory diseases where they are activated by non-allergic triggers, such as neuropeptides and cytokines, often exerting synergistic effects as in the case of IL-33. Mast cells can also release pro-inflammatory mediators selectively without degranulation. In particular, IL-1 induces selective release of IL-6, while corticotropin-releasing hormone secreted under stress induces the release of vascular endothelial growth factor.Once activated, mast cells secrete numerous vasoactive and pro-inflammatory mediators. These include pre-formed molecules such as histamine, serotonin, TNF, kinins and proteases stored in secretory granules. Leukotrienes (LT), prostaglandins and platelet activated factor (PAF) are synthesized during mast cell activation from arachidonic acid liberated by the action of phospholipases. In addition, a number of cytokines (e.g. IL-1, 2, 5, 6, 8, 9, 13, TNF) and vascular endothelial growth factor (VEGF) are synthesized de novo and released several hours after stimulation.

COMPLEMENT PROTEIN.

The complement system is a collection of blood and cell surface complement proteins that is a major primary defense and a clearance component of innate and adaptive immune responses. At least 30 different complement proteins act sequentially to produce a wide ranges of activities, from cell lysis to augmentation of the adaptive response. The complement system has four major antimicrobial functions.Activation of inflammation – Several peptides produced by proteolytic cleavage of complement proteins bind to vascular endothelial cells and lymphocytes. These cells then produce cytokines which stimulate inflammation and enhances responses to foreign antigens.The contribution of the pattern recognition system to complement activation assures the rapid initiation of the complement cascade as a part of an early immune response and inflammation. In fact, the activation of complement occurs immediately with high efficiency when the system encounters appropriate stimuli. For example, in infection induced by Leishmania, approximately 90% of promastigotes are lysed by complement in just 2.5 minutes after contact with human blood. Therefore, complement effectors generated as a result of this activation can participate in the earliest events of an inflammatory reaction

PHAGOCYTES : The main phagovytes involove during inflammatory response include neutrophils and macrophage. The serum and other compounds leaking from capillaries cause swelling of the area where pathogen has entered, which in turn causes pain. Various kinds of white blood cells are attracted to the area of inflammation. The types of white blood cells that arrive at an inflamed site depend on the nature of the injury or infecting pathogen. For example, a neutrophil is an early arriving white blood cell that engulfs and digests pathogens. Neutrophils are the most abundant white blood cells of the immune system.  Macrophages follow neutrophils and take over the phagocytosis function and are involved in the resolution of an inflamed site, cleaning up cell debris and pathogens.

ANSWER 3)

The lymphatic vasculature is not considered a formal part of the immune system, but it is critical to immunity. One of its major roles is in the coordination of the trafficking of antigen and immune cells.

• The lymphatic system plays a key role in the immune system, fluid balance, and absorption of fats and fat-soluble nutrients.
• As lymph vessels drain fluid from body tissues, this enables foreign material to be delivered to the lymph nodes for assessment by immune system cells.

Lymphatic endothelium in the lymph node participates in presenting antigen, most generally to promote peripheral tolerance but also to serve as a long-term reservoir for antigen presentation late in a response for the promotion of CD8+ T cell memory. A subset of lymphatic endothelial cells express peripheral antigens, or acquire them through uptake of dying cells, for subsequent MHC-I-mediated presentation to CD8+ T cells, leading to immunological tolerance. Lymphatic endothelial cells capable of long-term retention of antigens, such as viral proteins or particles, in lymph nodes undergo apoptosis during lymph node contraction in the late phases of an immune response. The dying lymphatic endothelial cells are engulfed by (DENDIRITIC CELL) DCs that cross-present foreign antigens originally present in lymphatic endothelial cells. This mechanism fosters the generation of CD8+ T cell memory against viral antigens