Immunology Physiology Flashcards
What are 2 main lineages of WBCs?
myelocytic lineage
lymphocytic lineage
What is the normal proportion of WBCs stored in bone marrow compared to circulation? How many days supply does to circulation provide?
6 days supply
3 times as many WBC in bone marrow
After being released from the bone marrow what is the granulocytes’ life span in the blood versus in the tissues?
hours (4-8 hours)
several days in tissues
What is the monocytes life span in the blood stream versus in tissues?
hours (10-20)
months
What is the life span of lymphocytes? How much time do they spend in the circulation at once?
weeks to months
just few hours
What is the life span of platelets?
10 days
What are the steps of neutrophil and monocyte extravasation?
margination
increased endothelial permeability
diapedesis
chemotaxis
Name examples of substances creating the Chemotaxis source
- DAMPs
- PAMPs
- complement cascade products
- clotting products
Chemotaxis is effective up to XXXXX micrometer.
100
List 3 mechanisms by which the phagocytic cells differentiate physiologic from pathophysiologic structures
- smooth surface of healthy tissues –> the rougher surface the more likely phagocytized
- healthy tissues are covered by protective protein coat - repell phagocytes
- pathologic structures identified by antibodies and complement (C3) - opsonization
What are the 2 major phagocytic cells?
macrophages
neutrophils
Describe the steps of phagocytosis by neutrophils or macrophages
identifies particle/bacteria etc –> attaches itself –> psuedopodia formed “hugging” the particle and engulfing it –> chamber formed –> breaks away from the cell surface and swims in the cytoplasm “phagocytic vesicle” –> lysosomes added to vesicle to digest particle –> released by exocytosis
List the digestive and bactericidal agents in phagocytic lysosomes
- proteases
- lipases (macrophages only)
- oxidizing agents (suproxide, hydrogen peroxide, hydroxyl ions)
List the components of the reticuloendothelial system
- monocytes/macrophages
- specialized cells in the endothelium, bone marrow, spleen, lymph nodes
Inflammation is characterized by the following 5:
- vasodilation –> increased blood flow
- increased capillary permeability –> fluid extravasation
- coagulation/ clotting of fluid in the interstitial space
- leukocyte accumulation (granulocytes and monocytes)
- tissue cell swelling
How is inflammation walled off? Describe how this differs between Staph and Strep bacteria
fibrinogen clots block of the lymphatics and tissue spaces
the more invasive/destructive the pathogen the quicker the wall-off response
* staph infection is causing severe damage but is walled off faster
* strep infection is more subtle initially and the walling off is slower –> strep more commonly causes hematogenous spread and death
Describe the steps of neutrophil extravasation
- adhesion molecules on endothelial surface (e.g., selectins, ICAM-1)
- neutrophils have integrins on surface making it stick to the endothelium
- loseing of capillary and small venule walls
- neutrophil squeezes through gaps - diapedesis
- chemotaxis attracts neutrophils
List th 5 most important factors in controlling the response of macrophages to inflammation
- TNF-alpha
- IL-1
- granulocyte-monocyte colony-stimulating factor
- GCSF
- MCSF
List 7 components of the innate immunity
- phagocytic cells
- stomach acid secretion
- skin barrier
- lysozymes in blood - attacks and dissolutes bacteria
- polypeptides in blood inactivating bacteria
- complement complex
- natural killer lymphocytes
Explain the difference between cellular and humoral immunity
both part of the adaptive/acquired immunity
cellular: T-killer cells
humoral: antibodies produced by B-lymphocytes
How do macrophages interplay with lymphocytes?
present antigens - digests pathogens and then presents parts of it as antigens - stimulate lymphocyte clone activation
macrophages can produce IL-1 –> promotes growth and reproduction of lymphocytes
What is the function of T-helper cells?
produce lymphokines - activate B lymphocytes
Describe the process of B cells producing antibodies
B lymphocytes are activated by macrophages –> start forming plasma cells –> produce large amounts of antibodies
What are memory cells?
B-lymphocytes that reproduce after initial insult and antibody production - at subsequent exposures a large amount of antibodies can be rapidly produced
Fill the gaps
What is the antibody-antigen coupling held together by? (4)
- hydrophobic bonding
- hydrogen bonding
- ionic attraction
- van der Waals forces
What is the affinity constant?
concentration of bound antigen-antibody complexes / antibody cc times the antigen concentration
What percentage of all antibodies do IgG constitute?
75%
When are IgM primarily produced and why are they so effective despite their small numbers?
during initial insult
have many antigen binding sites (10 compared to the 2 in IgG)
List the 4 ways by which antibodies can directly inactivate invading agents
- aggregation
- precipitation
- covering toxic site on surface - neutralization
- lysis
What are the 11 most important proteins of the complement system?
- C1 - C9, B and D
Draw the complement cascade (classical pathway)
List the 7 effects of the classical pathway of the complement system
- Opsonization, i.e., activates phagocytic cells - C3b
- lysis - membrane attach complex
- agglutination
- neutralization
- chemotaxis C5a
- mast cells and basophil activation - C3a, C4a, C5a
- inflammation
What is part of the membrane attack complex?
C5b6789
What has to be present on the antigen presenting cells in order for T lymphocytes to respond to them? What are its 2 types?
Major histocompatibility complex proteins (MCH)
MCH I - presents antigens to cytotoxic T cells/natural killer cells
MCH II - present antigens to T helper cells
What are the 3 main antigen-presenting cells?
macrophages
dentritic cells
b-cells
What are the 3 types of T cells?
T helper cells
Cytotoxic T cells
Suppressor T cells
What do T-helper cells produce?
lymphokines
How do cytotoxic T cells kill cells and what is another name for them?
- secrete perforins - hole forming proteins - “punch holes” in the membrane of the attacked cells
- fluid flows through holes into the cell - cell death
natural killer cells
Describe how IgE causes allergic rections
activates basophils and mast cells - cause rupture of these cells –> histamines, proteases, leukotrines, etc.
During an allergic reaction when basophils and mast cells rupture, what do they release?
- Histamines
- Eosinophil chemotactic susbtance
- Heparin
- Leukotrines
- Proteases
- Neutrophil chemotactic substance
- Platelet-activating factors
Describe type I hypersensitivity reactions
antigen exposure –> via skin, GI tract, respirtory tract –> activates antigen specific T helper cell subset –> stimulates B lymphocytes –> become plasma cells –> make a lot of IgE –> IgE binds to mast cells
reexposure –> antigen binds to IgE on mast cells, causes cross linking between two IgE –> triggers degranulation of mast cells
Explain type II hypersensitivity reactions
mediated by antibody-antigen binding
IgG or IgM against self-antigens on cell surfaces (e.g., RBCs, PLTs)
binding of Ag-Ab initiates complement cascade
* inflammation
* membrane attack complex
* opsonization of phagocytic cells
* natural T killer cells attracted
–> cell destruction
e.g., IMHA, ITP, myasthenia gravis
Explain type III hypersensitivity reactions
IgG formed against exposed antigen - IgG binds to antigen and forms AbAg complex - immune complexes then deposit in tissues and activate complement proteins - causing local inflammation
if not localized to a tissue but spreading through circulation (if antigen excess) –> can reposit in vascular beds of the kidneys, joints, eyes, skin
examples: FIP, glomerulonephritis, systemic lupus erythematosus, rheumatoid arthritis
Explain type IV hypersensitivity reactions
Antigens directly stimulate T helper cells - no antibody mediation
cell-mediated so takes longer (24-72 hours)
APC present antigent to T-helper cells –> produce cytokines attracting phagocytic cells –> tissue inflammation
examples: leishmaniasis, contact hypersensitivity, polymyositis, immune-mediated thyroiditis
