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Immuno Assignment 1 Answer.docx

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Health Sciences
Jonathan Bramson

1. Two intrinsic barriers that could prevent the pathogen from causing infection in the GI tract would be both physical and chemical barriers. When entering the GI tract through ingestion, the epithelia of the gastrointestinal tract provide a physical barrier that separates the internal milieu from foreign pathogens. The epithelia contain tight junctions that would prevent V. cholera from penetrating between the epithelial cells along the GI tract. As well the epithelia release mucus, a thick fluid that contains mucins (glycoprotein) that would trap the cholera pathogen and prevent it from adhering to the GI lining. Another barrier of the GI tract is the chemical substances released that inhibit the growth of pathogens. The upper GI tract releases bile salts, lysolipids, fatty acids and digestive enzymes that all create a difficult environment for pathogens to grow. Also along the intestinal (lower) portion of GI tract, there is the release of antibacterial proteins called cryptdins (form of α-defensin). 2. Lacking B-1 cells would affect the classical complement pathway. B-1 cells respond primarily to polysaccharide antigens from pathogens that result in the production of antibodies of the IgM class. These antibodies, known as ‘natural’ antibodies, are in high abundance in the body (even in the absence of infection) and bind primarily with the polysaccharide capsule of bacteria. This antibody:antigen complex then activates the classical complement pathway, resulting in the removal of the bacteria. Thus, if the B-1 cells are not present there is no production of the IgM antibodies and slower activation of the classical complement pathway (i.e. classical pathway can still be activated later on in the infection process when specific IgG antibodies bind with the pathogen forming another form of the antibody:antigen complex). 3. Healthy B-1 cells would be responsible for the production of natural IgM antibodies. The classical pathway, which recognizes and is activated by the binding of IgM to V. cholera, is beneficial because it takes a small initial signal and is able
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