Physio 2013: INFLammation and Immunity

The inflammatory response is characterized by increased vascular permeability, which allows fluid and immune cells to move from the bloodstream to the site of infection or injury. This increased permeability is necessary for the recruitment and emigration of leukocytes, such as neutrophils and macrophages, which are key immune cells involved in the inflammatory response. Additionally, phagocytosis of antigens and debris by these immune cells helps to clear the infection or repair damaged tissue. This option accurately describes the components that characterize the inflammatory response.

Neutrophils make up 60-80% of the leukocytes. Macrophages are 3-8%. Lymphocytes (NK, T, B) are 20-30%. Erythrocytes are red blood cells.

B and T cells are part of the adaptive immune response.

IgG makes up 80% of the antibodies. It is the smallest, most mobile (can most easily escape the bloodstream into the interstitial fluid).

B cells, specifically plasma B cells, become antibody producing factories with the help of cytokines and T helper cells. These B cells secrete antibodies. Other B cells have antibodies bound to their surfaces (BCRS).

B cells can be either memory cells or plasma (effector) cells (described in a previous question). Memory and effector cells are the two groups of cytotoxic T cells as well. Effector T cells are the ones that perform the cytotoxic functions in T cells and the ones that produce antibodies in B cells.

Macrophages produce proteases that help in removing foreign protein from the wound, release thromboplastin to stimulate fibroblast activity and secrete peptide growth factors to facilitate growth of new blood vessels. "They are like the maggots of the immune system" - CDR O.

The classical pathway is usually triggered by IgG or IgM antibody-antigen complexes (triggered at C1). The alternative pathway is normally triggered by lipopolysaccharide or bacterial endotoxins (started at C3). The alternative pathway is continuously activated, like a car engine that's idled. The lectin pathway is triggered by a biomolecule called lectin and can also be triggered on first exposure (triggered at C2 and C4).

Any nucleated cell can process and display antigen with MHC I proteins. This path of antigen-presentation happens with intracellular antigens. MHC II antigen presentation is for extracellular antigens that are engulfed by phagocytes.

Macrophages are immune cells that play a crucial role in the immune response. They have various receptors on their surface that allow them to recognize and respond to different signals. Fc receptors are present on macrophages and are involved in antibody-mediated immune responses. Selectins and integrin receptors are also present on macrophages and are involved in cell adhesion and migration. Cytokine receptors are present on macrophages and are involved in the response to cytokines. However, muscarinic receptors are not typically found on macrophages. Muscarinic receptors are primarily found in the nervous system and are involved in mediating the effects of acetylcholine.

IL-2 is the correct answer because it is released by TH1 helper cells and plays a crucial role in activating other immune cells such as helper T cells, cytotoxic T cells, NK cells, and macrophages. It is also required by cytotoxic T cells to perform their function effectively. This cytokine is important for coordinating and regulating the immune response against pathogens.

Class II Major Histocompatibility Complex (MHC) proteins are used for antigen presentation on dendritic cells, macrophages, and B cells. These cells are part of the immune system and play a crucial role in recognizing and presenting antigens to T cells. Dendritic cells are specialized antigen-presenting cells that capture and process antigens, macrophages are phagocytic cells that engulf and present antigens, and B cells are responsible for producing antibodies against specific antigens. By presenting antigens on MHC class II proteins, these cells activate T cells and initiate an immune response against the antigens.

Antibodies are part of the humoral, or blood, immunity and do not enter tissue. That's why we need other mechanisms (e.g, neutrophils and macrophages).

Macrophages secrete a lot of cytokines that initiate inflammation and chemotaxis (e.g., IL-10, IL-12, IL-6, TNF-alpha; See p. 165 in Copstead). T helper cells similarly release many cytokines (see p. 167). While mast cells also release cytokines during degranulation, macrophages and T helpers are the primary sources.

The coagulation cascade is linked to the inflammatory response primarily to block off the infected area and prevent spread.

Factor XII, also known as the Hageman factor, is considered the intersection of coagulation and immunity. This factor plays a crucial role in both the coagulation cascade and the activation of the immune system. It is involved in the initiation of blood clotting by activating other clotting factors and promoting the formation of fibrin. Additionally, Factor XII is also involved in the activation of the immune system, as it can trigger inflammatory responses and contribute to the defense against pathogens. Therefore, Factor XII acts at the intersection of both coagulation and immunity.

During an inflammatory response, mast cells release various vasoactive chemicals. Histamine is one of the primary chemicals released by mast cells and it causes vasodilation and increased vascular permeability. Prostaglandins, another vasoactive chemical released by mast cells, also contribute to vasodilation and increased vascular permeability. Leukotrienes, which are lipid mediators, are also released by mast cells during inflammation and they play a role in increasing vascular permeability and promoting the recruitment of inflammatory cells. Therefore, the correct answer is Histamine, Prostaglandins, and Leukotrienes.

The second answer somewhat describes the mechanisms of phagocytosis by macrophages and neutrophils, which do not apply to T cytotoxic cells. The third answer is wrong because T helper cells only recognize MHC II complexes.