BLD 204 EXAM 2 QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026

BLD 204 EXAM 2 QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026 what is immunity? - Answers - protection against infection - freedom from a harmful condition - immune system is made up of the cells and molecules that defend the body against pathogens antigens - Answers molecules recognized as non-self (epitope is recognized) - endogenous: native to self - exogenous: environmental antibodies - Answers also know as immunoglobulins (Ig) - one monomeric unit is 2 identical heavy chains and 2 identical light chains coming together to form 2 AB binding sites - five classes based on heavy chain structure and how many monomeric units they have what do antibodies do? - Answers - agglutinate and lyse bacteria - opsonize bacteria - initiate classical complement pathway - neutralize toxins - block microbe entry into tissues - assist in killing infected cells *not all classes do all of these* function of antigen presenting cells - Answers - capture and display the Ag flag - three types: DC dendritic cells, macrophages, and B cells function of dendritic cells (DC) - Answers capture and present antigen to T cells - express MHC II and T cell costimulatory molecules - found in the T cell zones in lymphoid tissue function of macrophages - Answers phagocytize and present antigen function of B cells - Answers recognize antigen via BCR, take it in and process it, present via MHC II molecules to helper Ts MHC class I - Answers - present on nucleated cells - signal to CD8+ cytotoxic Ts - heavy α chain and β2 microglobulin chain MHC class II - Answers - present on professional APCs - antigen is consumed, processed, and presented in MHC II by these cells - two peptide chains of more equal size - signal recognized by CD4+ helper Ts IgG - Answers - 70-80% of plasma Ig - monomeric - diffuses out of vasculature - neutralizes toxins and opsonizes bacteria - only class that crosses placenta *found in blood* IgM - Answers - largest, a pentamer - units joined together at Fc fragments by J chain - 10 binding sites, good for repeated isotopes - first after immunization IgA - Answers - mucosa, tears, sweat, bile, breast milk - dimer, J chain connection - stops bacteria and viruses from entering epithelium IgE - Answers - Fc fragment binds to receptors on mast cells - Ag-binding results in release of granules (histamine, leukotrienes) and calls eosinophils - parasite infections - involved in hypersensitivity IgD - Answers - present on some B cells - helps with antigen recognition/activation along with IgM primary lymphoid tissue - Answers - thymus and bone marrow - cells differentiate and mature into lymphocytes here secondary lymphoid tissue - Answers - lymph nodes, spleen, MALT - adaptive immune responses develop here T cell functions in cell mediated immunity - Answers CD8+ - involved in direct killing of cells - cytotoxic Ts - cytokine production cytokines involved in immunity - Answers - innate immunity and inflammation: TNF, IL-1, chemokines - regulate lymphocyte responses and functions in adaptive immunity: IL-2, IL-4, IL-5, IL-6, IL-10, IFN-gamma - stimulate hematopoiesis: GM-CSF, G-CSF, M-CSF, IL-3 innate immunity - Answers - made up of cells and molecules that are always ready to provide a defense against invaders - not antigen specific - components: epithelial barriers, pH, phagocytes (neutrophils and macrophages), natural killer cells, circulating proteins *fast, but non-specific* natural killer cells - Answers - lymphocytes - cytotoxic - recognizes loss of MHC I self molecules on cells that are malignant or virus infected adaptive immunity - Answers - cells and molecules that can respond to the microbes that got away from innate protection - specific and powerful - humoral and cell mediated humoral vs. cellular immune responses - Answers humoral: B cells recognize a specific antigen with BCR and produce antibodies that circulate blood, can take a while cell mediated: MHC I presents antigen to CD8 T cells (cytotoxic) that are activated, which identify and destroy infected cells isotope (class) switching - Answers - constant (C) region of the heavy chain is changed to another type - antigen specificity remains the same - switch to IgG, IgE, or IgA is dependent on cytokines *changes B-cell's production of antibody from one class to another* what are the ways that antibodies combat microbial infections - Answers - neutralize bacteria and their toxins by binding to them - opsonization (tagged to be killed by phagocytes) - ADCC (antibody dependent cell mediated cytotoxicity) - activation of complement (which results in lysis and more opsonization, and inflammation) T-cell dependent B-cell activation - Answers - most antigens aren't able to activate B cells - they need T helper (CD4+) lymphocytes to develop response *B-cells can act as APCs* - BCR recognizes antigen - antigen is ingested and chopped up - pieces are displayed on MHC II surface THEN - CD4+ T helper cells recognize that presented antigen *T helper cell produces cytokines that stimulate B cell proliferation and differentiation T-cell independent B-cell activation - Answers - multiple copies of the antigen are present close together and engage multiple BCRs on a cell surface - stimulates proliferation of B-cell line, differentiation into plasma cells and antibody production - antibodies are IgM (no switching to other antibody types) - doesn't result in memory (will not be prepared for next attack) how do B and T cells respond to such a variety of antigens? - Answers due to somatic recombination during lymphocyte development cell mediated immunity - Answers cytotoxic T cells - MCH I presents antigen to CD8+ T - CD8+ T is activated - CD8+ T interacts with cell that presents antigen - CD8+ T stimulates apoptosis in infected cell humoral immunity - Answers antigen recognition - B cell recognizes a specific antigen with their BCR hypersensitivity reactions: type I - Answers immediate, allergy, reagin-activated - Th2, IgE, and mast cells are central to this response - first exposure to antigen/allergen + Th2 helper cells are activated and influence class switching to IgE production + lots of IgE is produced if person is susceptible (due to genetics) + binds to mast cells via Fc portion = sensitized (ready to respond to antigen) - second exposure to antigen/allergen + mast cells release mediators from granules and synthesize others from lipids (histamine, proteases, prostaglandins, leukotrienes) + also secrete cytokines (TNF, chemokines, IL-4, IL-5, IL-13) + symptoms depend on how antigen exposure happens (hay fever symptoms, bronchospasm, conjunctivitis, dermatitis, hives, GI upset, anaphylaxis) *A = allergy, histamine reaction* hypersensitivity reactions: type II - Answers C = cytotoxic hypersensitivity or antibody mediated - antibody against some tissue component epitope is key here - antibody binds to epitope: three outcomes that lead to destruction + phagocytosis + complement activation + antibody dependent dysfunction - clinical outcomes depend on antibody specificity + immune hemolysis: hemolytic disease of the newborn due to Rh + drug induced: drug acts as carrier for a hapten, drug unmasked something that antibody could bind + Graves disease: TSH binds to receptors on thyroid, releases hormones when not needed, metabolism goes into overdrive *antibody to bind to a receptor causing dysfunction of a cell type by blocking or stimulating receptor activity* hypersensitivity reactions: type III - Answers I = immune complex mediated - antigen/antibody complexes are the main problem - size of complexes influences outcomes - amount of antigen and antibody matters too - a lot of AB/AG complexes form and deposited into tissue + large complexes usually get cleared pretty well + lots of antibody and the deposit is usually local + lots of antigen and the depositing is more widespread because the smaller complexes are more soluble - once deposition happens, THAT causes inflammation (10 days after antigen or so) + complement activation + vasoactive amines + platelet aggregation - outcomes: vascular smooth muscle damage (fibrinoid necrosis) - ex. + glomerulonephritis if deposition is there + arthritis if deposition is in joints + serum sickness: large amounts of foreign proteins for passive immunization, specific antibody formed, complexes with circulating antigen, and it is deposited in various tissues hypersensitivity reactions: type IV - Answers D = delayed type hypersensitivity - cell mediated - sensitized T cells do the damage - ex. reaction in TB test + happens 12-48 hours after exposure + T effector cells secrete cytokines + prolonged response becomes granulomatous inflammation - cytotoxic lymphocytes + kill cells showing the antigen + rejection of transplants occurs through this mechanism - outcomes: inflammation (contact dermatitis), granulomatous inflammation, tissue/organ rejection