Immunity Flashcards
(27 cards)
Survival of organisms
- eliminate foreign invaders and threats
- infectious pathogens, damaged tissues
- inflammation is protective mechanism
- “innate immunity”
First line of defense
Innate Immunity nonspecific barriers -physical (mucus membrane) -mechanical (hair, cilia) -biochemical (enzymes)
Second line of defense
inflammation
still part of innate
histamine released
macrophages activated
Third line of defense
specific immunity
cell-mediated (T-cells) vs. antibody-mediated (B-cells, plasma cells, APCs)
memory
Characteristics of inflammation
Dolor, rubor, calor, tumor
Transudates
fluid leakage
hydrostatic pressure increased
colloid osmotic pressure decreased
Exudates
fluid and protein leakage
chemicals included in vascular changes in inflammation
vasodilation-histamine
capillary permeability-histamine, kinins, vascular endothelial growth factor (VEGF), vascular permeability factor (VPF)
Steps to inflammation
recruitment
activation
chemotaxis
Types of inflammation
Serous (blister)-effusion
Fibrinous-more extensive, within body cavities, fibrinogen appears
Suppurative (purulent)-pyogenic (pus): microbe present, abscesses: local, superlative
Ulcer-errosion of tissue/organ surface, necrotic tissue
Cell-derived mediators
Vasoactive amines-histamine (vascular permeability), serotonin (homeostasis and clotting)
Eicosanoids-prostaglandins, prostacyclins, thromboxanes, leukotrienes, vasoactive, bronchiospasm, chemotaxis
Complement-capillary permeability, vasodilation
Kinin and coagulation-homeostasis, complement activity
Characteristics of chronic inflammation
mononuclear infiltration
tissue damage
healing-repair, angiogenesis, fibrosis
Cells in chronic inflammation
leukocytes: neutrophils, monocytes->macrophages
lymphocytes: B & T cells
Eosinophils
Mast cells
Granuomatous inflammation
walling off
giant cells
epitheloid cells
Lymphocytes
develop in lymphoid organs
B-cells: bone marrow
Thymus: T-cells become immunocompetent here
Central tolerance
T-cells: trap in thymus, signal apoptosis, so not self-reactive
B-cells-in bone marrow, trap and kill
Peripheral tolerance
T-cells: self-reacting molecule escapes
-3 solutions
1. if no costimulation, anergy-nothing happens
2. apoptosis if activation takes place too quickly
3. least understood-suppressor/regulatory T-cells dampen response
None for B-cells
APCs
Antigen-presenting cells
B-cells
Macrophages
Dendritic cells (CD4/MHC-II, CD8, MHC-I)
Five types of Ig
IgA dimer-high in blood, body
IgD monomer-low in blood, on B-cells, activate basophils & mast cells, produce antimicrobial factors
IgE monomer-lowest in circulation, mediates allergic response, responds to parasites
IgG monomer-80-85% in circulation, crosses placenta, breast milk
IgM pentamer-
Direct ways to combat antigens
Neutralization
Agglutination-clumps antigen
Precipitation-precipitate out of blood if soluble
Indirect ways to combat antigens
Opsonization-antibody binds to pathogen, label as foreign
Phagocytosis-act of engulfind and digesting foreign body
Inflammation-triggered by complement cascade, trigger neutophils, enzymes, ROS intermediates
Which of the following is NOT a correct pairing? A. CD4+, helper T cells B. CD8+, MHC-I C. CD4+, MHC-II D. Plasma cell, antibody E. APC, fibroblast
E. APC, fibroblase
After degranulation, mast cells release prostaglandins and leukotrienes that perform what functions?
A. Vasodilation and increased vascular permeability
B. Attraction of CD8 cells
C. Activation of the Complement cascade
D. Opsonization of bacteria
E. Three of these occur
A. Vasodilation and increased vascular permeability
B-Cell immune deficiency diseases
X-linked agammaglobulinemia (Bruton disease)
-S&S: low/absent (b-cells/plasma cells), normal t-cell response
Selective IgA deficiency
-recurrent infections, most common
