Immunology Exam 1 Practice PDF

**[Immunology Exam 1 Practice]** **1. Introduction to Immunology** Explain the differences between the innate and adaptive immune systems. (include responses, cells, proteins etc) Give a limitation for each of the innate and adaptive immune systems. Describe the cellular origins of neutrophils,...

**[Immunology Exam 1 Practice]** **1. Introduction to Immunology** Explain the differences between the innate and adaptive immune systems. (include responses, cells, proteins etc) Give a limitation for each of the innate and adaptive immune systems. Describe the cellular origins of neutrophils, macrophages, dendritic cells, B cells, T cells and NK cells. Where are B and T cells generated? Where do they develop? Give two examples of a secondary lymphoid organ and explain the substructures and what is found within them. Describe the differences in structure between BCRs, TCRs, and immunoglobulins. Describe flow cytometry. Which T helper cells are associated with the response to the following infections: helminth, influenza, staphylococcus, mycobacteria. **2. Innate Immunology** Give an example of two PRRs from different families that would detect an extracellular gram-negative bacteria. Generally, what would they sense and signal. What are the major cell types in the innate immune system and what are their functions? What are the roles of IL-8 and TNF-a? What cells make them? Explain the signals that dictate NK cell activity. Give an example of signals present when NK cells kill and when they don't. Explain the process of extravasation. What is the difference in function between M1 and M2 macrophages. Which TLRs detect pathogens in the endosome vs outside of the plasma membrane? Explain the relationship between these location groupings and the PAMPs they recognize. What are defensins and how do they work? What is a transcription factor activated by TLR signaling? What does it promote? **3. MHC and Antigen Processing** Describe the structural differences between MHCI and MHCII including where they bind the peptide, TCR, and costimulatory proteins. Describe how many MHCs can one person express? Explain. Explain from pathogen to TCR recognition how the different MHC responses work. (Include cell types, cellular locations, and major proteins) Explain which CDR regions of a TCR bind where and why this explains the location of TCR variability. Explain generally why tissue graft rejection happens and the direct and indirect mechanisms of rejection. **4. B Cell Development and Antibodies** What are the functions of antibodies? Explain all the steps of VDJ recombination for BCRs. What are the different stages of B cell development. In each stage, what does the BCR germline DNA look like, is there a BCR being expressed? Explain the different possible outcomes for autoreactivity testing for B cells. **5. T Cell Development and Activation** Describe the biological/mathematical need for VDJ recombination.  How does the recombination of the alpha chain vs the beta chain of a TCR differ?  Other than the combination of different segments encoded in the germline DNA, what else contributes to TCR diversity? What about immunoglobulins? Compare and contrast TCR vs BCR antigen recognition. Describe the steps of T cell development after generation in the bone marrow. Where do positive and negative selections occur? (include substructures of organ, what part of TCR is rearranged and is being expressed) Is T cell lineage fate (either CD4+ or CD8+) dictated by strength of TCR binding? How do organ specific self-antigens get selected against in the thymus? If this didn't happen what would the result be? What is the function of an MHC/peptide tetramer?  \*Explain the steps of TCR signaling starting from the initial interaction with an APC. How does the BCR signaling differ? \*What are the major costimulatory and counter regulation pathways in T cells. Give one example of how this pathway is utilized for clinical disease treatment. Where does the activation of naïve T cells occur.  Why does a second exposure to a pathogen result in a more robust T cell response? Why is this not the case for chronic infections?