innate and adaptive immunity Flashcards
innate immunity is
non-specific
has no memory
includes first line of defense: physical structures and chemical secretions.
and
second line of defense: phagocytic cells, NK cells, antimicrobial prtiens, inflammatory response.
adaptive immunity is
specific! tailors its fight in response to antigens.
has memory
third line of defense:
1. lymphocytes: B and T cells, leukocytes(WBCS) and dendritic cells (APC)
2. antibodies: trigger the classical pathway.
3. macrophages and other APC’s.
HUMORAL (B CELLS) AND CELLULAR (CD4 AND CD8 T CELLS)
types of granulocytes
neutrophils
basoophils
eosinophils
mast cells
types of agranulocytes
monocytes: macrophages and dendrites
dendritic cells
natural killer cells: lymphocyte
B-cells: lymphocyte
T-cells: lymphocyte
WBCS include
neutrophils
lymphocytes (b cells and t cells)
monocytes/macrophages
eosinophils
basophils
basophils
granulocyte + innate
release histamines
inflammation + allergic reactions
eosinophil
granulocyte + innate
kill parasites with oxidative burst (some are phagocytic)
mast cell
granulocyte + innate
APC.
release chemicals to activate inflammation
neutrophil
granulocyte + both systems
phagocytize bacteria and fungi
first at the site of the initial INFX.
monocytes
granulocyte + both systems
become macrophages
cause inflammation and perform phagocytosis
dendritic cells
agranulocyte + both systems
present antigens to T-cells, initialing the adaptive immune response
APC and phagocytic.
NK cells
agranulocytes + both systems + lymphocyte
kill cancer cells and virus-infected cells
plasmocyte - B-cell
agranulocyte + innate + lymphocyte
APC cells!
recognize antigens and produce antibodies.
T-cells
agranulocyte + innate + lymphocyte
secrete cytokines
*CD4 - MHC-II. T-helper cells
*CD8 - MHC-I. recognize and kill “non-self cells”. cytotoxic T-cells
complement system:
classical
alternaitve
lectin
C3 protein then leads to
cytolysis
opsonization
inflammation
classical pathway
uses antibodies produced by CD4 t-helper cells TH2, released by interleukin 4, activating a B-cell (humoral response), which become plasma cells, activating the compliment system classical pathway.
C1
C2 & C4
C2a & C4b
C3
alternative pathway
lipid-carb complex
C3
lectin
lectin proteins.
C2 & C4
C2a & C4b
C3
cytolysis
C3
C3b
C5
C5b
cell rupture with C6 7 8 9
opsonization
C3
C3b
enhances phagocytosis and promotes adherence.
inflammation
C3
C3a & C3b
C5
C5a & C5b
releases histamine by binding to mast cell.
vasodilation and increased permeability of Vs.
inflammatory response + fever + vasoactive mediators.
activated by MHC-I
(MHC - major histocompatibility complex: cell surface proteins that present antigens to cells)
cd8 cells.
cytotoxic cells.
activated by a virus-infected cell.
induce apoptosis by releasing perforin to attack and destroy the cell.
intercellular.
activated by MHC-II
(MHC - major histocompatibility complex: cell surface proteins that present antigens to cells)
cd4 cells.
t-helper cells.
dendritic cell (APC)
activates TH-1, TH-2, and TH-17
CD4 TH-1
release interleukin-2 and interferon gamma
activate cd8 cells & macrophages (phagocytes)
CD4 TH-2
release interleukin-4
- activate eosinophils - kill parasites
- activate humoral response/extracellular. B-cells activate to become plasma and memory cells to produce antibodies to bind to the epitope region of the antigen/microbe.
- causes the direct antibody killing of microbe, activating the classical pathway of the complement system.
- activates mast cells and basophils! C3a + C5b receptors release histamine, causing an increase in vascular permeability and the inflammatory response.
CD4 TH-17
release interleukin-17
- activate neutrophils, which are high during the early stages of INFX.
promote the inflammatory response.
neutrophils fight fungi and extracellular bacteria.
colonel selection + expansion
selection: B-cell identifies the antigen.
expansion: B-cell proliferates/cells divide.
interleukins
cytokines that serve as communication between WBCS
interferons
interfere with the viral INFX of host cells.
antibody class switching
the initial IgM response switches to a more specific antibody, like IgG.
phagocytosis
done by neutrophils and monocytes/macrophages.
1. chemotaxis
2. adherence
3. ingestion
4. digestion
inflammatory response
- vasodilation: increase the permeability of BV’s. vasoactive mediators
- phagocytosis: neutrophils and macrophages
- tissue repair: stroma and parenchyma
PRISH symptoms.
