Adaptive Immune System Flashcards
what are two types of adaptive immunity
Antibody mediated (humoral) immunity cell-mediated immunity
what is an antigen
old definition ‘antibody generator”
new definition: any molecule that reacts specifically with Ab or Ag receptor on lymphocyte
does not necessarily induce IR
what is an immunogen
Ag that can induce IR
Antigenic/ immunogenic
relative ability of Ag to elicit IR
Antigenic determinants=
epitopes
discrete regions of Ag molecule specifically recognized by adaptive IR
e.g. stretch of 10 or more AA
e.g. 3D structure/protusion in a molecule
antigenic structure
Antibody-mediated (humoral) immunity
what is the main component
produced by
antibody is the main component
produced by B-lymphocytes =B cells (develops in Bursa of birds, bone marrow in humans)
neutralizes free-floating particles (bacteria, toxins and viruses)
in response to extracellular Ag, B cells triggered to proliferate and differentiate into plasma cells
Y-shaped proteins called Abs
some B-cells form memory cells that respond faster when exposed to the same antigen again
Antibody structure
two functional regions
2 identical arms and 1 stem
Arms- bind to specific antigen (Fab)
Stem -tags antigen for destruction by other IS components (Fc- binds phagocyte)
Light chain
two types based on amino acid sequence of the constant regions
λ and k
A given B cell will produce Ab of only one specificity
Both L chains are identical, so either both will be Lλ or Lk
Heavy chain
five types based on AA sequence of the constant region, gives the 'class' of the antibody type µ = IgM γ = IgG α = IgA δ = IgD ε = IgE
γ = IgG structure
makes up 75% of serum immunoglobulins has basic monomeric structure four subclasses based on amino acid sequence of the C regions of the H chains IgG1, IgG2, IgG3, IgG4 IgG1 is most prevalent
γ = IgG functions
opsonization -enhances phagocytosis, acts as a flag for phagocytes when Fab is bound to antigen and Fc is freely exposed
neutralizes viruses and toxins
main Ab type made in secondary response, when body encounters Ag for a second and subsequent times
crosses placenta -passive immunity for fetus from mother
µ = IgM structure and functions
Monomeric, when attached to B-cell surface as a receptor
it is pentameric in serum, 5 monomers held together by a J chain
First Ab class produced in primary response
Ag receptor on B cells
activates part of innate defenses
agglutinates particulate Ag e.g. bacteria
δ = IgD
monomeric form
Found in serum and on B cell surface as receptor
very low amounts, <2% of total serum Ab
unknown function -back-up incase IgG non-functional or not made????
α = IgA
primary Ab produced by cells of the mucus membrane
secretory Ab, found in mucosal secretions
Low amount and monomeric form in serum
Dimeric in secretions
Functions:
neutralizes bacteria and viruses by preventing them from attaching to mucus membranes
passive immunity in breast milk
ε = IgE
monomeric form, low levels in serum
Ag receptors on Mast cells (tissues) and basophils (blood)
functions: anaphylactic hypersensitivity
how is the classical complement pathway activated?
when Ab binds to an Ag -activates C1
converts it to C1qrs: splits C4 and C2 farming C4b2a = C3 convertase (similar to C3bBb in alternative pathway)
remaining events same as alternative pathway
C3 convertase splitting C3 into C3b and C3a (which together with C5a act as anaphylatoxins)
C3b binds to microbe-Ab compex and remaining components join in (C5b, C6, C7, C8, C9) to form MAC attack
Role of T-Lymphocytes
activation and summary
T-cells, Cell-mediated immunity -mature in thymus
Do not recognize free Ag, rather Ag must be presented by one of body’s own cells e.g. bacterial or virally infected cells, transplant tissues, cancer
Bind to peptide derived from intracellular organisms complexed with Major Histocompatibility Complex (MHC) molecule
T-cell receptor (TCR) binds the complex of MHC molecule and peptide
T-lymphocytes are activated
T-lymphocytes help macrophages kill intracelllular parasites
T helper type 1 (Th1) + Class 2 MHC -> T-cell release macrophages activating factors (IFNγ), NO radicals
Two major functional population of T-cells
surface markers (cluster of differentiation)
cytotoxic T cells
Helper T cells
Cytotoxic T cells
differentiate into Tc which destroy infected or cancerous cells -CD8 recognize Ag presented by MHC class 1 molecules
Helper T cells
differentiate into Th which activate B cells and macrophages -CD4
Th1 -activate macrophages
Th2 -activate B cells
recognize Ag presented by MHC class 2 molecules
difference in structure for MHC 1 and 2
MHC class 1 3 alpha subunits and one beta2m
MHC class 2 two alpha and 2 beta
Role of T-lymphocytes once activated
T-lymphocytes help macrophages kill intracellular parasites
Th1 cells + Class 2 MHC -> T-cell release macrophage activating factors (IFNγ) -no radicals
T-lymphocytes inhibit intracellular replication of viruses viral infected cells express class 1 MHC recognized by Tc cells
what is the lymphoid system
what is it designed to do, what does it contain
collection of tissues and organs designed to bring B an d T cells into contact with Ags that enter the body
lymphocytes are highly specific, only recognize 1 or 2 Ags -essential that approriate lymphocyte encounters given Ag to mount effective IR
lymphoid vessels -carry lymph
Primary Lymphoid organs
what happens here
bone marrow and thymus
hematopoietic stem cells develop into B and T cells
both B and T cells originate in bone marrow but only B cells mature here, T-cells mature in thymus
once matured, lymphocytes gather in secondary lymphoid organs waiting to encounter Ag
encapsulated secondary lymphoid organs -> immune response
lymph node-> to antigens in tissues
spleen -> to antigens in blood
unencapsulated secondary lympoid organs -> immune response
MALT -> to antigens at mucosal surfaces
secondary lymphoid organs
site where lymphocytes gather to collect Ags
e.g. lymph nodes, spleen, tonsils, adenoids, appendix
situated at strategic positions in body to capture Ags
e.g. lymph nodes capture ags from lymph, spleen captures from blood
after lymphocytes make contact with Ag they proliferate forming clones of cells specific for that Ag
some lympoid organs less organized
MALT -prevents invasion from mucosal surface
SALT -prevents microbes invading skin
Difference in surface markers
CD molecule (cluster of differentiation)
B-cells -surface immunoglobulin
T-cells -T-cell receptors (TCR)
Clonal selection and expansion of B-lymphocytes
as lymphocytes mature in primary lymphoid tissue, a population of cells generated that are able to recognize limitless variety of Ags
each individual cell is able to recognize and respond to 1 epitope
body is estimated to have 1 billion B cells but only a few recognize a given epitope
how does clonal selection and expansion work for B-lymphocytes
what prevents IS from acting against itself
Only B cells capable of making corret Ab bind to Ag = “clonal selection”
Cells that bind Ag begin dividing, produce population of clones= “clonal expansion”
somatic mutations for further selection
most lymphocytes require 2nd opinion (accessory signals) from another cell (Th cell) before activation to occur, prevents IR against self
clonal selection and expansion of T-lymphocytes
similar to B cells
some of these cells release cytokines, others have cytotoxic function
no further selection as a result of somatic mutations
a fraction of clonally expanded population differentiates into memory cells
t memory cells CD45RO
b memroy cells CD27 and surface IgG,A or E
memory cells
more readily stimulated by antigen
greater combining power
B cells through mutation and selection
T cells, increased expression of accessory adhesion molecules
basis for the principle of vaccinations
two types of T-independent antigens
polyclonal activators
repeating determinants
don’t need a Th cell to give a second response.
cytokines
soluble intercellular communication factors
important role in protection against infectious diseases
- control of infection
- development of pathology
cytokines -> interferons
a viral infected cell will produce interferons to bind to an uninfected cell and induce that cell to produce anti-virals
cytokine production helps define T-helper subsets by
mutual antagonism between two subsets
autoregulation of immune system
