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HMX Immunology Final Exam Study Guide 2022 With Complete Solution

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HMX IMMUNOLOGY FINAL EXAM STUDY GUIDE

1. Tissue resident sentinel cells include (3 types): Dendritic
cells, macrophages, and mast cells

2. Circulating leukocytes involved in innate response (2 types):
Monocytes and neutrophils

3. Phagocytic immune cells (2 types): Macrophages and neutrophils

4. Difference between macrophages and neutrophils?: Neutrophils are
short lived and will undergo apoptosis after eating a microbe;
macrophages are longer-lived and will eat apoptotic cells and waste

5. General cytokine role in innate immune response (and what cells release
them?): Released by dendritic cells, macrophages, and mast cells. Pro-
inflamma- tory molecules that interact with blood vessel endothelium
to recruit circulating leukocytes, fluid, and proteins into tissue

6. Which tissue-resident sentinel cell will release histamine upon
activa- tion?: Mast cell

7. Cytokines promote up-regulation of what kind of molecule within
blood vessel walls?: Adhesion molecules

8. E-Selectin: An adhesion molecule that helps to slow down
circulating leuko- cytes in innate immune response (low-affinity
interaction)

9. E-Selectin Ligand: A ligand expressed by circulating leukocytes
that helps them stick to blood vessel endothelium in innate
immune response


,10.ICAM-1: An adhesion molecule that helps circulating leukocytes
bind to blood vessel endothelium in innate immune response (high-
affinity interaction)

11.Integrins (and the name of a specific one): A class of adhesion
molecules expressed on circulating leukocytes; LFA-1 binds to ICAM-1
in a high affinity interaction during the innate inflammatory response

12.Stable Arrest: When a circulating leukocyte comes to a stop
within the en- dothelium thanks to adhesion molecule interactions
and can enter the tissue

13.Pus: Comprised of fluid and apoptotic cells/waste as a result of an
inflamma- tory response (DNA, dead bacteria, apoptotic neutrophils)

14.Psoriasis overview: Autoimmune disease that can cause skin
plaques and arthritis; Skin plaques are caused by immune cells
migrating into the skin and initiating an inflammatory response

15.Psoriasis risk factors: History of strep infections, skin injury, first
degree relative with psoriasis






, 16.TNF-alpha in psoriasis: A pro-inflammatory cytokine expressed in
psoriasis that recruits immune cells into the skin and also acts directly
on epithelial cells to produce thickened/raised patches

17.Psoriasis treatment (biologics): Target the pro-inflammatory
cytokine TNF-alpha and therefore prevent the expression of
adhesion molecules on en- dothelial cells and prevent TNF-alpha
from acting directly on epithelial cells

18.Possible side effects of medications that block adhesion molecules:
Sus- ceptibility to infection due to inhibiting leukocyte entry into tissue

19.Most abundant leukocyte: Neutrophils

20. What kind of infections are neutrophils particularly effective against?: -
Extracellular bacterial infections

21.Plasmacytoid dendritic cell: A type of sentinel cell that detects
viruses and releases type 1 interferons

22.Type 1 Interferons (Type 1 IFNs) function and the cell that is most
efficient at producing them: Group of cytokines that activate the
antiviral state during viral infection; Plasmacytoid dendritic cells

23.The Antiviral State: Protective state that cells enter in response to
Type I Interferons; proteins that can bind to viral double-stranded
RNA are produced, infected cells will die, RNAse activity is induced

24.Pathogen-associated molecular patterns (PAMPs): Molecules that are
commonly expressed on pathogens but not vertebrate cells, help
distinguish self from non-self; can be on cell surface or released from

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