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22 Cards in this Set

  • Front
  • Back
Adaptive Immune Responses Are Agenic - What is an Ag?
mcls presented by MHC proteins and recognized by TCRs and ABs

usually made up of different epitopes (Agic determinants) each of which binds a specific Ab
Ag and Agic Determinants Key Concept
For every Agic determinant there is a specific AB capable of reacting to it
Cell Mediate Immunity
for KILLING cells with INTRACELLULAR pathogens

cytotoxic T lymphocytes
macrophage activation
Humoral Mediated Immunity
Controlling EXTRACELLULAR pathogens

C cells
plasma cells
Pepsin monomers and Fc
degrade Fc of immunoglobulin, get only Fab dimer
Papain
2 Fab
IgG
80% total Ig circulating in blood

passive immunity: only AB that can pass placenta

enhances phagocytosis

neutralizes toxins and viruses
IgM
first AB to appear following infection, fastest

IgM + IgG important for recruitment of complements
IgA
mucosal AB

important in host defense at mucosal surfaces

present in breast milk
IgE
key role in hypersensitivity rxns (allergies)

defense against parasitic infections
IgD
found on surface of B lymphocytes

B cells bind to AB

M and D are only isotypes that can be expressed in same cell
Antimicrobial action of ABs
opsonin: enhance phagoytosis

neutralizes viruses and toxins (block att)

agglutinate bact = aid in clearing

render orgs non motile

- activ complement path
Allergy: what happens?
capillary and airway diation
pain
mucosal secretion
What are allergies?
immune system overreacts, hypersensitive

mediated by IgE

releases histamines and prostaglandins
Process of allergic rxn
1: first time, make large amounts of allergen AB

2: IgE att to mast cells

3: 2nd exposure, IgE primed mast cells rel. granules like histamine and cytokines

4: mount allergic respons
What is asthma?
inflammatory disorder of airways

causes wheezing, short of breath, tightness, coughing
Role of IgE in asthma
IgE and allergens bind to mast cell which triggers degranulation and inflammatory mediators
Cause of asthma
genetic
certain resp infections as infant
contact with some airborne allergens or viral infections early childhood
NK cells
innate immunity

killing tumor cells and viruses

release small cytoplasmic granules of protein - perforin and granzymes --> apoptosis
How do NK cells recognise targets?
MHC I can be lost during infection or result of malignant transformation

NK have Fc receptor on surface

When NK cells encounter AB coated host cells lacking MHC II --> degranulates, causing cell to apoptose
How does the body distinguish self from pathogens?
MHC proteins

- function as AP mcls that interact with Ag and TCR

- MHC I ALL nucleated cells
- pres Ag to CD8 cytotoxic T cells

- MHC II ONLY APC --> DCs, Macrophages, B cells
- pres Ag to CD4 Helper T

After MHC pres, Ag processing pathway is dif - CMI or HMI (ab)
Inflammatory Response
localized accumulation of fluid, blood proteins, phagocytic cells

- anaphylatoxins and other loc. rel. mcls recruit more phagocytic cells

- phag cells move to site via chemotaxis or diapedesis (pass thru intact vessel walls)

- phag cells prod. cytokine and chemokine