The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by:  The inability of active C3b to diffuse away in the blood plasma. The inability of active C3b to covalently attach to the membranes of eukaryotic cells. The rapid hydrolysis of active C3b in solution, rendering it inactive. The tight binding of active C3b to the C3 convertase. The ability of active C3b to recruit phagocytic cells.

NCR- ILC3 make up one of the most frequent ILC subsets in the human peripheral blood, while NCR+ ILC3 are virtually absent in the circulation during homeostasis. Importantly, the healthy human intestine hosts dominantly NCR+ILC3, which have been shown to be essential in maintaining gut homeostasis. The signature cytokine of NCR+ ILC3 is IL-22. ILC3 in mice sense their environment and control gut defense as part of a glial-ILC3-epithelial cell unit orchestrated by neurotrophic factors. Enteric ILC3 express the neuroregulatory receptor RET. ILC3-autonomous Ret ablation led to decreased innate interleukin-22 (IL-22), impaired epithelial reactivity, dysbiosis and increased susceptibility to bowel inflammation and infection. Does this this complex neuro immune cross talk in the intestine account for the NCR ILC3 cells producing IL-22 while no such associations exist in the circulation where the ILC3 cells are NCR- and produce IL-17? maybe O yes O no

The small fragments of some complement proteins initiate a local inflammatory response.  Recent studies using mouse models of pulmonary inflammation (a model for human asthma) have found that mice deficient in the C3a receptor have greatly reduced disease symptoms when challenged with inhaled preparations containing extracts of the fungal pathogen Aspergillus fumigatus. Specifically, the C3a receptor-deficient mice showed reduced influx of granulocytes and lymphocytes into the lung and reduced fluid in the lung after challenge. What is the explanation for these findings?

Please explain why

True or False: FHL patients show increased susceptibility to infection because secretion of IFN-γ in cytotoxic granules is impaired.   True or False: Autoimmune-like symptoms of patients with complement deficiencies are due to the complement pathway’s normal functions in clearing immune complexes from the circulation.

The mechanism of cross-presentation by dendritic cells is an essential pathway for generating CD8 T cell responses to some intracellular pathogens. If this pathway did not exist, we would be highly susceptible to: Intracellular pathogens that can survive inside macrophage endocytic vesicles Intracellular pathogens that are able to evade antibody responses Intracellular pathogens that do not infect and replicate in dendritic cells Intracellular pathogens that can spread from cell to cell by inducing cell fusion Intracellular pathogens that infect and replicate in red blood cells

A 55-year-old male was diagnosed with rheumatoid arthritis (RA) after experiencing complications from an infection during his youth. Rheumatoid arthritis is an autoimmune disease that manifests as chronic inflammation, primarily in the joints. The patient states that he manages his symptoms well and lives a lifestyle that attempts to keep the inflammation at a minimum. (CD4 T helper cells and other immune cells in a patient with RA promote cytokine release, especially release of interleukin-1 (IL-1) and tumor necrosis factor (TNF)). Inflammation is a natural immune response, providing immediate defense against foreign invasion. However, when not controlled, inflammation can cause damage to normal, healthy tissue. This patient is most likely to present with which of the following clinical signs and symptoms during a typical visit to his primary care provider? Choose the correct answer and provide a brief explanation. (2-3 sentences) a). Fever b). Redness, pain, heat, and swelling of…

TLR-4 recognizes bacterial lipopolysaccharide in association with the host accessory proteins MD-2 and CD14. True/False: All mammalian TLRs have been shown to directly bind to microbial products, leading to TLR signaling.

Which of the following proteins downregulates the classical complement cascade by breaking up the C3 convertase into individual C4b and C2a units? O Protectin (CD59) O Lectin O C1 Esterase Inhibitor O Decay Accelerating Factor (CD55) O MASP

Individuals infected with herpes simplex virus (HSV) mount protective antibody responses directed against surface glycoproteins of the virus.   These antibodies are critical to viral clearance.  The act to neutralise any virus trying to infect a person’s cells as well as activating the classical pathway of complement and cytotoxic cell-mediated killing of infected target cells. Having a deficiency in the complement component C3 greatly impairs a person’s ability to control HSV infections.   To understand this further, you will investigate this in the lab.  Using C3-deficient mice, you infect them with HSV at day 0 and then a second time 4 weeks later.           A hypothesis is a tentative answer to a scientific question and is an important part of practical experiments.  A testable hypothesis is statement that can be proved or disproved as a result of experimentation.   Q1. State the problem that you are trying to solve. And then formulate a robust testable hypothesis for your…